Russian Journal of Genetics, Vol. 40, No. 9, 2004, pp. 945–958. Translated from Genetika, Vol. 40, No.

9, 2004, pp. 1157–1172.

Original Russian Text Copyright © 2004 by Chadov, Chadova, Kopyl, Artemova, Khotskina, Fedorova.

THEORETICAL PAPERS
AND REVIEWS

From Genetics of Intraspecific Differences to Genetics

of Intraspecific Similarity
B. F. Chadov, E. V. Chadova, S. A. Kopyl, E. V. Artemova,
E. A. Khotskina, and N. B. Fedorova
Institute of Cytology and Genetics, Russian Academy of Sciences, Novosibirsk, 630090 Russia;
e-mail: chadov@bionet.nsc.ru
Received October 16, 2003

Abstract—Based on the Mendelian approach to heredity, modern genetics describes inheritance of characters
belonging to the category of intraspecific difference. The other large category of characters, intraspecific simi-
larity, stays out of investigation. In this review, the genome part responsible for intraspecific similarity is con-
sidered as invariant and regulatory. An approach to studying the invariant part of the Drosophila melanogaster
genome is formulated and the results of examining this genome part are presented. The expression of mutations
at genes in the invariant genome part is different from that of Mendelian genes. We conclude that these genes
are present in the genome in multiple copies and they are functionally haploid in the diploid genome. Severe
abnormalities of development appearing in the progeny of mutant parents suggest that the mutant genes are
genes regulating ontogeny. A hypothesis on an elementary ontogenetic event is advanced and the general
scheme of ontogeny is presented. A concept on two types of gene allelism (cis- and trans-allelism) is formu-
lated. This approach opens a possibility for studying genetic material responsible for the formation of intraspe-
cific similarity characters at different taxonomic levels on the basis of crossing individuals of the same species.

INTRODUCTION
In line of the basic idea of the founder of genetics,
Gregor Johannes Mendel, modern genetics studies
characters of living organisms and factors controlling
them. Hereditary factors (in modern terms: genes, DNA
regions) are studied exclusively by genetics, whereas
characters are subject matter of both genetics and biol-
ogy in general. It is important to understand the mean-
ing of the term character in context of biology and
genetics and thus the nature of cooperation of these sci-
ences in this area.
According to a formal logic definition, “A character
is anything in which objects or phenomena are similar
to or different from one another; a characteristics or a
feature of an object or a phenomenon by which they can
be recognized and distinguished” [1]. Characters inher-
ent only to the given object or phenomenon are called
distinguishing, and those inherent to many objects, gen-
eral or nondistinguishing [1]. As applied to biological
objects, individuals of the same species possess both
distinguishing and general characters. General charac-
ters determine the intraspecific similarity; distinguish-
ing, the intraspecific difference(s).
In the categories of intraspecific similarity and
intraspecific differences, words similarity and differ-
ence are antonyms, but in the living organism, charac-
ters of these categories supplement rather than exclude
each other, creating the general phenotypic appearance
of the species. The intraspecific similarity category
should not be confounded with similarity by a charac-
ter. For instance, two pea plants with yellow peas are
similar in the pea color, but this is similarity in the cat-
egory of intraspecific difference: a representative sam-
ple of the species Pisum sativum would contain plants
with peas of other colors. The two trait categories
greatly differ biologically. Intraspecific differences do
not hinder crosses with fertile progeny, whereas differ-
ences in intraspecific similarity characters present an
insurmountable barrier for crossing.
The intraspecific difference characters may be
hereditary and nonheritable. The intraspecific similar-
ity category has a more complex structure, including
hereditary characters of all taxonomic ranks, from the
species and higher. For example, for the species Pisum
sativum L., which was the object of Mendel’s experi-
ments, the intraspecific similarity category includes:
(1) characters characterizing all living matter
(exchange of substances and energy with non-living
matter, existence in two states: living and dead, ability
to reproduce, etc.); (2) characters of the plant kingdom
(e.g., photosynthesis); (3) characters of legumes (e.g.,
nodules); and, finally, (4) characters of the species
proper, Pisum sativum, distinguishing it from all other
species of the family Leguminaceae.
To study heredity, Mendel suggested tracing inherit-
ance of characters only of the intraspecific difference
category and only clearly heritable ones. He left out
non-heritable (individual) characters from the intraspe-
cific difference category and the whole category of
intraspecific similarity. The rediscovery of Mendel’s laws
kindled a dispute on their universal nature. Some biolo-
gists, while positively evaluating Mendel’s approach,

1022-7954/04/4009-0945 © 2004 MAIK “Nauka /Interperiodica”

946 CHADOV et al.
doubted the applicability of his laws to heredity in gen-
eral, which included not only alternative characters of
intraspecific difference but also all other traits [2]. For
instance, Timiryazev counted 18 character types, out of
which only one, in his opinion, showed Mendelian
inheritance [3]. Filipchenko argued that macroevolu-
tion is based on biological traits that do not follow Men-
del’s laws rather than on Mendelian characters [4, 5].
De Vries believed that quantitative characters are
beyond the scope of Mendelian approach (cited from
[6]). The claims of the universal nature of the Mende-
lian models were quite reasonable encountered by the
issues of the genetic basis of numerous non-alternative
characters, of specific inheritance of sex, etc.
The modern genetics failed to preserve the rational
core of these doubts. Genetic literature either avoids
biological interpretation of the notion of character or
equates character to with difference, thus simulating
Mendelian approach to the character study. The history
of genetics shows multitudes of attempts to find solu-
tions to biological problems without accounting for the
fact that a large group of biological characters was not
yet subjected to genetic analysis and that their genetics
may prove different from the traditional model based
on intraspecific difference characters. In general, the
approach to the gene–character issue is as follows: any
character is complex; it is formed under the influence of
many genes including major (limiting) genes and mod-
ifiers [7]. This approach does not account for qualita-
tive difference between the characters; non-Mendelian
inheritance is explained only by the gene number and
their interaction. All genes are thought to be Mendelian,
that is, possessing properties revealed by Mendelian
analysis. It is generally believed that the cases of non-
Mendelian inheritance will be explained as our knowl-
edge on ways of implementation of a gene into a char-
acter expands [2]. Here, the existence of any other
genes except Mendelian ones is again ignored. It is nat-
ural that for the early geneticists who developed the
methods of tracing inheritance, the issue of intraspe-
cific similarity was redundant. However, genetics of the
late 20th century, which proclaims its universality, can-
not overlook it. The results of complete sequencing of
genomes directly pose the problem as to whether the
unknown function of most of genetic material is related
to the fact that the Mendelian method and the genetics
based on it could not reach genes of very important cat-
egories.
On the strength of the modern genetic knowledge,
including the results of the studies considered below,
the universal nature of the Mendelian laws is regarded
as follows. The use of characters of intraspecific differ-
ence led to the discovery of the general regularities of
inheritance together with regularities characteristic
only of this category of characters. The aim of the mod-
ern genetics lies, in particular, in determining which of
the regularities are general, and which are specific, and,
of course, in finding the genetic basis of the intraspe-
cific similarity characters. It is clear that the old meth-
RUSSIAN JOURNAL OF GENETICS
odology, which was designed for working with
intraspecific differences, here will be of no help.
There are two genetic fields to resolve this problem.
The first of them is the genomic text. This text repre-
sents all genes, and it is of importance to find the func-
tion of each of these genes [8]. The second field is char-
acters of an individual. As shown above, each individ-
ual presents a set of characters of all taxonomic levels.
In any cross, all characters are transmitted to the prog-
eny. The problem is that Mendel developed an algo-
rithm for heredity analysis for genes of intraspecific
difference, whereas for genes of intraspecific similarity,
this algorithm is yet to be designed.
INVARIANT PART OF THE GENOME
AND THE METHOD
OF CONDITIONAL LETHALS
The existence of two categories of characters poses
a question on the genetic basis of this distinction. At the
present stage of development of genetics, there is no
doubt that the characters in either of the categories are
controlled by genes located on the chromosomes, the
chromosomes segregate in meiosis according to Men-
del’s rules, and each diploid individual receives a hap-
loid chromosome set from each of its parent. However,
for some reasons some characters exhibit variability
while others are uniform. The whole biological taxon-
omy is based on the uniformity of characters. The vari-
ability is genetically explained by existence of a gene in
different variants, or alleles. The simplest explanation
of the uniformity would be the absence of gene alleles,
i.e., genetic monomorphism. A striking phenotypic
similarity of monozygous twins results from their iden-
tical genotypes.
Studies of protein polymorphisms in natural popula-
tions revealed the existence of monomorphism for a num-
ber of proteins in fairly representative samples [9–11].
These findings were accompanied by the facts of the
absence of allele dynamics in populations during long
periods of time [12–15]. These groups of results led to
a rejection of the leading role of allele polymorphism in
evolutionary transformations [16, 17]. Altukhov has
advanced a hypothesis on the existence of an invariant
genome part playing a key role in the determination of
interspecific differences. Based on the results of the
long-term studies in comparative population genetics,
this author as early as in the 1970s came to the conclu-
sion that “one of the most important properties of the
eukaryotic genome is duality of its structural and func-
tional organization, which is directly reflected in two phe-
nomena: polymorphism and monomorphism” [16, 17].
Although, as noted by Altukhov himself, the duality of
the structural–functional organization of genes or char-
acters of an organism was suggested earlier, e.g., by de
Vries, Goldsmidt, and Ushakov (cited from [16]), only
a discovery of many cases of protein monomorphism
permitted seriously pose the question on the existence
of an invariant part of the genome. Genetic monomor-
Vol. 40 No. 9 2004
 FROM GENETICS OF INTRASPECIFIC DIFFERENCES
phism of the species and duality of the structural orga-
nization of the eukaryotic genome has been currently
shown at the DNA level [18]. Note, however, that the
genetic community in general still believes that poly-
morphism is a property of each gene.
From the genetic viewpoint, the existence of an
invariant genome part means the following. In individ-
uals composing the species, all invariant genes must be
homozygous. If a variant arises through mutation, it
must perish immediately, i.e., in heterozygote. Each
mutation at genes of the invariant part of the genome
must be a dominant lethal.
The death of a mutation in a heterozygote signifies
that the gene cannot change. From the general biologi-
cal viewpoint, the absence of changes in this part of the
genome is equal to the banishment of evolution. There-
fore, it was attempted to find a way to combine the
death in homozygote with the possibility of altering the
gene. It was assumed that mutations in these genes
appear in the homozygous state. This state rescues the
mutation while the heterozygote state for it means per-
ishing. The mutation must behave as a conditional
dominant lethal: be lethal in heterozygote and non-
lethal in homozygote. The putative mutations with the
paradoxical properties were termed facultative domi-
nant lethals [19].
First, individuals homozygous for such mutation
(and thus viable) should be obtained, and then the
mutations should be tested for lethality in heterozygote.
If successful, this method would produce a collection of
dominant lethal mutations for further analysis, as is
done in genetics for all mutations. As Drosophila has
heterogametic sex determination, this procedure can be
applied to X-chromosomal mutations. Conditional
lethals are known in Drosophila and some other organ-
isms but for them external factors are the “conditions”
[20]. In our case, the conditions are genetic (genetic
background). In 1999, a method of obtaining condi-
tional lethal mutations has been developed for Droso-
phila X chromosome [21, 22], and then for autosome 2
[23]. Another method has been additionally designed
recently (Chadov, Khotskina, unpublished). Since all
these methods are based on a common principle, they
may be collectively termed the method of conditional
lethals.
THREE PROTOCOLS OF PRODUCING
CONDITIONAL LETHALS IN DROSOPHILA
MELANOGASTER. THE DIFFERENCE
OF THE CONDITIONAL LETHALS METHOD
FROM THE CLASSICAL SCREENING
FOR MUTATIONS
Protocol 1. Drosophila males are exposed to γ-irra-
diation and crossed with females carrying attached
X chromosomes (attached-X females) (Fig. 1). Male
progeny of this cross carry an irradiated X chromosome
and a haploid set of irradiated autosomes. Each of the
RUSSIAN JOURNAL OF GENETICS Vol. 40 No. 9
947
sons is individually crossed with females of the yellow
strain. A daughterless male is considered to carry a
mutation in the X chromosome. To preserve the muta-
tion, this male is crossed with females carrying
attached or inverted X chromosomes [21, 22].
The presence of an X-chromosomal mutation in the
male genome is not lethal, but the mutation becomes a
dominant lethal when it is in a female genome.
Protocol 2. Drosophila males are exposed to γ-irra-
diation and crossed with females carrying inversion
Curly in chromosome 2 (Fig. 2). Male progeny of this
cross carrying an irradiated autosome 2 and autosome
Curly are individually crossed with females of the yel-
low strain. A male that did not produce phenotypically
normal sons and daughters (without Curly) is consid-
ered to carry a mutation in autosome 2 [23].
Mutation in the male autosome 2 behaves in a dual
fashion: as a dominant lethal in a cross of the male with
yellow females and as a non-lethal, in a cross with
Curly females.
Protocol 3. Recessive lethal mutations in the
X chromosome are obtained in Drosophila by means of
the classical Muller-5 method. The lethals are maintained
by crossing In(1)Muller-5/lethal females with
In(1)Muller-5 males. In crosses of the females with
males of another strains, some lethals do not behave as
such, i.e., normal males appear. The appearance of
homozygous females carrying the “lethal” X chromo-
some is possible (Chadov, Khotskina, unpublished).
The mutations express as lethal only when the het-
erozygote at the lethal mutation is crossed with a male
carrying inversion In(1)Muller-5, while its lethal effect
disappears in a cross with a male not carrying this
inversion.
The main principle of isolating the mutations is as
follows: the presence of lethal effect of the mutation in
one genotype and the absence of this effect in another
one. According to protocol 1, the lethal effect is
removed by the presence of the mutation in a male
genome. In a female genome, the mutation is mani-
fested as lethal. According to protocol 2, the factor res-
cuing from the lethal effect of the mutation in autosome 2
is the presence of the inverted Curly chromosome.
Without this chromosome, both mutant sons and
mutant daughters die. Protocol 3 leads to an opposite
situation: the lethal effect of the mutation in the X chro-
mosome of the progeny is caused by the presence of an
inverted X chromosome in the paternal genome.
The classical method of isolating mutations is based
on a different principle: the mutation must stably
express in any individual of the given species. No clas-
sical procedure of isolation of mutations includes test-
ing their expression. It is stable expression that makes
possible maintaining collections of mutations for their
further use in crosses with various representatives of
the species. Mutations of the invariant genome part,
according to the method of their isolation, are unusual:
2004
948 CHADOV et al.
3000 Gy
XXY × X Y
X X × X Y
Individual
testing X X × X Y
of males
X X × X* Y
F1 Norm: daughters X X sons X Y
*
Mutation[*]: daughters X X sons X Y
Fig. 1. Detection of conditional dominant lethals in the X
chromosome of D. melanogaster. Exposed to γ-radiation
males were crossed with females carrying attached X chro-
mosomes. The male progeny were individually crossed with
yellow females. The sons having received the X chromo-
some with a dominant lethal were daughterless. The irradi-
ated X chromosomes are boxed; the X chromosome carry-
ing a new lethal is marked by an asterisk.
their expression assumes extreme values 0 and 1
depending on the genetic background.
FEATURES OF ORGANIZATION
AND EXPRESSION OF GENES
OF THE INVARIANT PART OF THE GENOME
Using the three protocols, we have isolated about hun-
dred mutations in Drosophila melanogaster. X-chromo-
somal mutations obtained following protocol 1 are
characterized in most detail. They differed from com-
mon mutations in a number of properties: (1) sharply
different penetrance in hybrids from crosses with dif-
ferent strains; (2) unclear relationship between the
mutant and normal allele; (3) different manifestation in
germline and somatic tissues; (4) dependence of the
expression of the sex of the parental donor of the muta-
tion; (5) mass formation of morphoses; and (6) frequent
reversions to the norm [24, 25]. Below, we consider the
properties that most clearly reveal the specific organiza-
tion and functions of the mutated genes.
1. The haploid genome bear several gene copies
(cis-alleles), only one of which is active in the given
individual. X-chromosomal mutations isolated by pro-
tocol 1 are maintained using two procedures. Accord-
ing to the first procedure, mutant males of the wild-type
phenotype are crossed with females C(1)DX, y w f /Y
RUSSIAN JOURNAL OF GENETICS
3000 Gy
×
In(2LR)Cy/2 2 /2
2/2 × 2 /In(2LR)Cy
Individual
testing 2/2 × 2 /In(2LR)Cy
of males
2/2 × 2*/In(2LR)Cy
Norm: 2/ 2 and 2/In(2LR)Cy
F1
Mutation[*]: 2/ 2* and 2/In(2LR)Cy
Fig. 2. Detection of conditional dominant lethals in auto-
some 2 of D. melanogaster. Exposed to γ-radiation males
were crossed with females carrying a complex inversion
and dominant marker Curly in one of autosomes 2. The
male progeny carrying this autosome and the irradiated
autosome 2 (in a hatched box) were individually crossed
with yellow females. The sons that had received autosome 2
with a dominant lethal produced only Curly progeny. Chro-
mosome 2 carrying a new lethal is marked by an asterisk.
carrying attached-X chromosomes. In this procedure,
the sons receive the mutant X chromosome from their
father. According to the second procedure, the mutant
X chromosome is maintained in heterozygous females
with the inverted Muller-5 chromosome. The female is
crossed with males carrying either mutant or inverted
X chromosome. Here, the sons receive the mutant
X chromosome from their mother.
The mutation behaves differently depending on its
maternal or paternal inheritance. If a son received a
mutant X chromosome from the father, it is viable in the
presence of the Y chromosome and non-viable in its
absence (Table 1). If a son received the same mutation
(mutant X chromosome) from the mother, it is viable
both in the presence and in the absence of the Y chro-
mosome (Table 2).
This different relationship with the Y chromosome
may be explained by the fact that the genome contains
both the mutated gene and its copies (or alleles) able to
perform its function. Out of these alleles, only one
functions. In the given situation, one allele is mutant
and the remaining ones are normal. In a male that
received the mutation from the mother, the normal
rather than mutant allele functions, and thus this male
is viable regardless of the presence of absence of the Y
chromosome in its genome. As is known, a male with
the normal genotype is viable even when the Y chromo-
some is absent in their genomes [26]. In Fig. 3 showing
the organization of the regulatory genes as compared to
Vol. 40 No. 9 2004
 FROM GENETICS OF INTRASPECIFIC DIFFERENCES 949

Table 1. The effect of the Y chromosome on lethality of mutations received by sons from fathers [22]
Cross
C(1)y w f/Y ×  + Cross
C(1)y/0 ×  +
Number
of male culture total number proportion total number proportion
of progeny of XY males in progeny of progeny of X0 males in progeny
1 51 0.35 131 0.02
2 42 0.60 118 0.05
3 33 0.39 90 0.05
4 85 0.38 137 0.00
5 8 0.25 97 0.12
6 133 0.50 37 0.03
7 37 0.57 142 0.12
8 19 0.47 123 0.16
9 199 0.55 123 0.05
10 30 0.40 107 0.14
11 152 0.51 95 0.13
13 61 0.49 54 0.09
15 82 0.50 70 0.20

the structural gene, the former is depicted as consisting
of three cis-alleles, only one of which is active in the
given genome.
The method of mutation isolation is based on the
fact that the gene impairment is critical even in a het-
erozygous state. The rescuing factor is that in the geno-
types in which the allele is being isolated it “must be”
inactive. Its cis-allele is active. The mutation is pre-
served only due to the fact that it had occurred in a non-
functioning allele. This method may be called isolating
mutations in “sleeping” genes, that is, alleles not func-
tioning in the ontogeny of the given individual. Accord-
ing to the experimental results, genetic factors respon-
sible for switching one allele and suppressing another
are as follows (in addition to the maternal or paternal
origin of the mutation): (1) the sex of the individual;
(2) the presence of a chromosome rearrangement
(inversion, translocation); (3) the genotype of the cross-
ing partner [19]. Because of the presence of factors
switching on and off the mutant genes, these genes can
be assigned to the regulatory ones [27]. In Section 4
devoted to the description of morphoses, we show how
the genes fulfill their regulatory function by changing
the process of ontogeny.
2. Homologous genes located in different homologs
(in trans-position) function alone according to the prin-
ciple of allele exclusion. Alleles of a structural gene
function according to the “double work” principle.
Activity of both structural gene alleles is especially evi-
dent on electrophoregrams of its protein products. In
Fig. 3, both alleles of the structural gene are shown as
active, but only one out of two regulatory genes (in one
of the homologs) is depicted active. When a structural
and a regulatory gene are structurally diploid, the latter
gene is functionally haploid.
The conclusion on allele exclusion of the regulatory
gene in the opposite homolog [23] was drawn based on
the facts of exclusively dominant expression of the
mutations in heterozygote. In crosses between mutant
males carrying the mutation in the X chromosome and
yellow females, female progeny perished (dominant
manifestation of the mutation). In the cases when
females carrying the mutation were viable, heterozy-
gotes displayed disrupted meiosis (chromosome loss).
This anomaly was also dominant as it occurred in het-
erozygotes. Morphoses appeared in the progeny of het-
erozygotes for the mutation (Section 4). This mutation
manifestation was also dominant.
In some cases, the mutations did not manifest in het-
erozygote. This state, however, cannot be classified as
recessive. For instance, X-chromosomal mutations iso-
lated by protocol 3 in classical genetics are referred to
recessive lethals: they are manifested as lethals in males
with one X chromosome and not manifested as such in
females carrying one mutant and one normal X chro-
mosome. However, for the isolated mutations it
appeared that their lack of manifestation in heterozy-
gote was caused by the fact that these mutations are not
lethal in females rather than by suppression of the lethal
mutation effect by the normal allele. Females homozy-
gous for these mutations are viable. Consequently,
these mutations are in fact dominant lethals manifest-
ing only in male individuals.
Mutations in autosome 2 isolated by protocol 3 are
expressed as dominant lethals if a mutant male is
crossed with a yellow female. In the reverse cross
(mutant female × yellow male), they do not manifest as
lethals. As we see, the presence of lethality (dominant
expression of the mutation) and the absence of lethality
(“recessive” expression of the mutation) depend not on

RUSSIAN JOURNAL OF GENETICS Vol. 40 No. 9 2004

950 CHADOV et al.

Table 2. The effect of the Y chromosome on lethality of mutations received by sons from mothers* [22]
Cross
In(1)Muller-5, wa B/+ ×  y Cross
In(1)Muller-5, wa B/+ ×  C(XY), y B/0
Number
of male culture total number proportion of XY, total number proportion of X0,
of progeny + males in progeny of progeny + males in progeny
2 317 0.10 103 0.13
3 122 0.19 15 0.13
5 242 0.22 122 0.26
6 501 0.15 156 0.19
7 377 0.18 117 0.33
8 363 0.25 192 0.30
9 250 0.12 139 0.10
10 194 0.23 182 0.25
11 291 0.22 170 0.29
29 285 0.21 307 0.11
30 378 0.15 165 0.19
31 460 0.17 121 0.21
32 226 0.19 89 0.21
33 162 0.14 205 0.22
34 264 0.10 193 0.01
35 444 0.08 184 0.10
36 481 0.21 221 0.28
38 504 0.24 138 0.24
41 359 0.23 227 0.39
* Mutation is in chromosome +.

the opposite autosome 2 from the yellow strain. It
seems that the analyzed genes do not interact with the
gene in the homologous chromosome. The expression
of these genes follows the exclusion principle: the
activity of the gene in one homolog means the inactiv-
ity of its counterpart in the other homolog. Therefore,
the manifestation of each of these genes looks as dom-
inant.
Lethal mutations in autosome 2, isolated by protocol 2,
are carried by male and female heterozygotes bearing
mutant autosome 2 and inverted autosome In(2LR), Cy 0.
The mutation carriers are viable not because the muta-
tion is recessive but because the mutated gene “ought to
be” inactive in the genotype with inversion In(2LR), Cy 0.
The mutually excluding activity of two regulatory
genes located in front of each other in a pair of homol-
ogous chromosomes gives the heterozygote for a regu-
latory gene a theoretical possibility to have two differ-
ent phenotypic expressions.
Functioning according to the allele exclusion princi-
ple has serious consequences for a regulatory gene with
a signaling function. A mutant impairment of a func-
tionally haploid gene means death of the individual.
The mutation cannot be preserved in heterozygote as
happens with mutations at structural genes. This results
in monomorphism of regulatory genes in the popula-
tion. Thus, we have come to the statement with which
we started our search for the mutations.
The fact that we did not suspect at the beginning of
our work but have found in the process of the study was
the combination of gene monomorphism at the diploid
level with its polymorphism at the haploid level. The
existence of cassettes of cis-alleles in a haploid set is
polymorphism at the haploid level. The existence of cis-
alleles and the inactive state of most of them throughout
the individual development allows one to isolate and
maintain mutations of these genes. Most genes become
accessible for studying by hybrid analysis.
3. The regulatory gene mutation has several pheno-
typic manifestations during individual development.
Two alleles of a structural gene, as a rule, function in
pair: both are either active, or inactive. If they are both
active, three forms of their interaction are possible:
recessive, dominant, or semi-dominant. Whatever is the
case, it is important that there is only one of three forms
of interaction for an allelic pair of a structural gene. For
the mutations found in our experiments, another rule
holds: they are characterized by several forms of inter-
action. The progeny of one mating pair (female het-
erozygous for the X-chromosomal mutation crossed
with a male) includes: (1) viable sons and daughters;
(2) lethal zygotes perishing at the embryonic stage

RUSSIAN JOURNAL OF GENETICS Vol. 40 No. 9 2004

 FROM GENETICS OF INTRASPECIFIC DIFFERENCES
(white and brown eggs); and (3) progeny having pheno-
typic abnormalities (morphoses). Progeny of any geno-
type from this cross may fall into each class. The ratios
between the three classes depend on the mutation. The
proportion of morphoses is low—from several percent
to several tens of percent; the rest is lethal or normal
outcomes.
It could be assumed that we deal with individual
variability inherent to all organisms. However, the pres-
ence of a regulatory gene mutation increases the
expression of this variability. The proportion of zygotes
dying at early stages of development is greatly
enhanced; the number of phenotypic abnormalities is
so high that they appear even in very small progenies.
The phenomenon that in genetic work with common
mutations is present as the background (several percent
of dominant lethals, few cases of abnormalities in the
progeny) is markedly manifested in a study of regula-
tory mutations.
4. A gene functions in one cell, and its product, in
another one (maternal and paternal effects of mor-
phose formation). As noted above, the formation of
morphoses is a characteristic feature of the mutations in
question. These morphoses are developmental defects
of different degree, which in some cases does not
hinder eclosion, mating, or even reproduction. Devel-
opmental defects have been described for individuals
exposed to extreme environmental effects [28–32]. In
contrast to these exogenous morphoses, the morphoses
obtained in our study were termed endogenous [25],
since their appearance is caused by internal factors,
namely, gene impairment.
Our collection includes more than two hundred
color video pictures of morphoses, some of which are
presented in Fig. 4. Morphological defects involved all
body parts of the fly and in some cases were very pro-
nounced: the absence of half of the head; half of the
thorax; one, two, three, or four legs; one wing; external
genitalia. Formations of the homeotic type were
recorded: double arista, seventh leg, protrusions on
eyes, thorax, etc., as well as melanoma-like neoplasms
of various localization.
In contrast to visible mutations, the morphoses
(1) appear in part of the progeny at a frequency of sev-
eral percent to several tens of percent; (2) are not heri-
table; (3) are unilateral; (4) the morphological change
often bring the fly on the brink of survival, but even pro-
found morphological alterations may be accompanied
by normal viability and fertility.
The maintenance of X-chromosomal mutations
(Fig. 5) produces two types of progeny: one of them
carries the mutant X chromosome while the others lack
this chromosome. The formation of morphoses
involves paternal and maternal effects. A morphose
could be formed not only in the progeny carrying the
mutant paternal chromosome but also in the progeny
lacking it. Naturally, the presence of the mutation in a
RUSSIAN JOURNAL OF GENETICS Vol. 40 No. 9
951
Inactive gene
Homolog 1 A1 A2 A3 B1
Homolog 2 A1 A2 A3 B2
a1 a2 a3
Regulatory Structural
gene gene
Fig. 3. Organization of a structural and a regulatory gene. In
the diploid genome, the structural gene is represented by
two alleles, B1 and B2, located in homologous chromo-
somes (homologs 1 and 2) (trans-alleles). The activation of
the structural gene concerns both alleles. The regulatory
gene is represented by a cassette of three alleles, A1, A2,
and A3 (cis-alleles). Each of the alleles is activated by its
own transcription factor (respectively a1, a2, and a3). Acti-
vation of any of the three alleles leads to the same result:
activation of structural gene B. A property of the regulatory
gene is its activity in only one of the homologs. In homolog 1,
the regulatory gene is switched off: none of the alleles func-
tions. In homolog 2, the A3 allele is activated by transcrip-
tion factor a3; this allele, in turn, activates both alleles of the
structural gene (B1 and B2).
parent is the necessary condition for the morphose for-
mation in its progeny.
Maternal effect manifested in the progeny of
females carrying the mutant X chromosome (+) and
inverted Muller-5, B wa chromosome. The progeny that
received the mutant X chromosome from the mother
consisted of daughters +/B wa and wild-type sons (+).
The progeny that did not receive the mutant X chromo-
some from the mother consisted of daughters B wa/B wa
and sons B wa. In a group of seven X-chromosomal
mutations obtained in a separate experiment (protocol 1),
all mutations produced morphoses in the progeny. Five
mutations exhibited maternal effect in the morphose
formation. Twenty-six progeny of flies carrying these
mutations (daughters B wa/B wa and sons B wa) had
morphoses although they did not receive the mutant
X chromosome from the mother.
In a group of 24 mutations isolated by protocol 3,
morphoses were recorded in the progeny of all mutant
females Muller-5, B wa/+. Out of 157 progeny with
morphoses, 73 (46%) did not receive the mutant
X chromosome from the mother. Of them, 30 were
females and 43, males. The morphose formation in the
progeny and the presence of the mutant X chromosome
in the same progeny seem to be independent events.
The formation of morphoses without receiving the mutant
X chromosome from the mother was also recorded in spe-
cial crosses of mutant females +/Muller-5, B.
Paternal effect was found in the cultures containing
attached-X females (females C(1)DX, y w f/Y) and
mutant wild-type males (+). In these cultures, sons
2004
952 CHADOV et al.

(a) (b)

(c) (d)

(e) (f)

(g) (h)

Fig. 4. Endogenous morphoses in D. melanogaster. (a) Sack-like protrusion on the midline of thorax; (b) absence of the right wing
with a necrosis focus at the wing base; (c) an additional third metathoracic leg; (d) the absence of the right thorax half; (e) partial
absence of the right metathoracic leg; (f) absence of tarsus and metatarsus of the left metathoracic leg; (g) absence of bristles on the
right thorax side, absence of the left wing; (h) absence of four legs, deformation of a leg and a wing.

receive the mutant X chromosome from the father, and
daughters, attached-X chromosomes lacking the muta-
tion, from the mother. The paternal effect manifested in
the appearance of daughters with morphoses. In the
group of seven mutations mentioned above, the pater-
nal effect was manifested in four mutations (22 mor-
phoses). The paternal effect was also observed in
crosses of mutant males with other females carrying
attached-X chromosomes. These were daughters with
morphoses that did not receive any mutant X chromo-
somes. Two out of seven mutations exhibited both
paternal and maternal effects.
In a group of 29 mutations obtained by protocol 1
and producing morphoses in progeny, morphoses were
detected by one visual examination in the daughters of

RUSSIAN JOURNAL OF GENETICS Vol. 40 No. 9 2004

 FROM GENETICS OF INTRASPECIFIC DIFFERENCES
26 mutants. As noted above, daughters did not receive
the mutant chromosome from father. The experimental
data indicate that the pathological phenotype (morphose)
of the progeny of the mutants without inheritance of the
mutant gene is a rule rather than an exception.
The mutant genes, as we have seen, demonstrate
both the maternal and the paternal effects. Apart from
sex of the parent, these effects are phenomenologically
indistinguishable. The maternal effect is generally
explained by cytoplasmic inheritance of gene products.
However, in case of the paternal effect, the cytoplasmic
inheritance of gene products is impossible. The regula-
tory products produced by the gene in the sperm X
chromosome, can be transmitted to the zygote only by
being fixed on the sperm autosomes. Therefore, the
explanation of both paternal and maternal effects is
beyond cytoplasmic inheritance. We believe that these
effects are explained by distinction in time and space of
two processes: production of the regulatory protein and
realization of this protein product. The distinction in
space means that the regulatory protein is produced in
one cell and realized in another cell of the next genera-
tion. The distinction in time means that the production
of the protein is not accompanied by its realization; the
latter process starts after the former is completed.
These results suggest that the mutant genes produce
the proteins that are initially inactive. The products of
the maternal genes appear in the oocyte, the product of
the paternal genes, in the spermatocytes; however, both
start functioning only in zygote. Thus, the regulatory
protein produced by the genes in question is “exported”
to function in other cells. In case of the classical gene,
the gene is active at the same place with its product. The
presence of a mutant phenotype signifies the presence
of the mutant gene. The classical genetics would simply
be impossible if the location of the gene functioning
with regard to protein production would differ from the
location of realization of this gene product.
Summarizing, using classical hybrid analysis we
found a large part of the genome consisting of regula-
tory genes. These genes are cardinally different from
typical genes in both organization and function. Appar-
ently, their role in the organism is also specific.
INVARIANT GENOME PART HOSTS
THE PROGRAM OF INDIVIDUAL
DEVELOPMENT
1. The genetic basis of the common program of indi-
vidual development in species members. Severe defects
of morphogenesis in the mutant progeny indicate that
the regulatory genes control ontogeny. The properties
of the mutations reveal the principles of this control.
The first principle is the non-alternative character of the
individual development program. The elimination of
mutant variants is ensured by functional haploidy of the
corresponding genes; the mutations are eliminated as
dominant lethals. The presence of the mutations in the
RUSSIAN JOURNAL OF GENETICS Vol. 40 No. 9
953
(a) (b)
In(1)M-5 In(1)M-5
y v f
+
× ×
+ y v f
In(1)M-5
In(1)M-5
In(1)M-5
F1
F1 + +
In(1)M-5
+
Fig. 5. Two methods of maintaining X-chromosome muta-
tions. (a) In heterozygote in females carrying inverted chro-
mosome Muller-5 (In(1)M-5) and mutant X chromosome
(+, bold line); (b) in a culture with attached-X chromosomes
(y v f/y v f). In the first case (a), the mutant X chromosome
is transmitted to daughters In(1)M-5/+ and sons +; daugh-
ters In(1)M-5/In(1)M-5 and sons In(1)M-5 do not receive
this chromosome. In the second case (b), the mutant chro-
mosome is transmitted to sons but not daughters.
organism is possible until the mutant allele becomes
active. Variants of the process of ontogeny are possible
owing to the occurrence of the regulatory gene in form
of a cassette consisting of cis-alleles. However, the
number of these alleles is lower than the number of
combinations of trans-alleles of structural genes in the
process of population hybridization.
2. Cell mechanism of information quantization in
ontogeny. To construct a scheme of genetic control of
ontogeny, we may reasonably presume that this control
is based on a chain of sequential activation of regula-
tory genes [33]. The problem here lies in the fact that
each cell contains the whole genome; therefore, with-
out assuming an activation-limiting mechanism, we can
come to an absurd conclusion that the total genome is
active in zygote. Based on the discovered property of
the ontogeny-controlling genes, we propose a mecha-
nism of quantum genome activation (Fig. 6). An essen-
tial feature of this mechanism is that switching the
activity of one gene to another depends on the cell divi-
sion as an obligatory condition.
The production by an ontogeny gene of the regula-
tory protein product, which will function only after the
cell division, at the given time restricts the activity of
the cell genome to one ontogeny gene. The transmis-
sion of activity from this gene to another one occurs
only after the cell division. To make the scheme valid,
an ontogeny-controlling gene must possess a function
of starting cell division. On the scheme, this function is
shown by the hatched arrow.
We called an elementary ontogenetic event a transi-
tion of activity from one ontogeny-controlling gene to
another through a cell division [34]. The event is mul-
tiply repeated and thus controls three ontogenetic pro-
2004
954 CHADOV et al.

(a) (b) (c)

Fig. 6. Transition of activity of a regulatory gene in the maternal cell to the activity of another regulatory gene in the daughter cell
(an elementary ontogenetic event). (a) The original cell with two chromosome pairs. The active and inactive regulatory genes are
shown as solid and open squares, respectively. The active regulatory gene and its inactive product create an impulse for cell division
(hatched arrow). (b) Mitotic cell division. Inactive gene products are dispersed in the cytoplasm. Circles with rays, spindle poles.
(c) Two daughter cells. The division switched off the previously active regulatory gene (open square), and, activating the regulatory
product received from the maternal cell (solid circles), switched on another regulatory gene. Open triangles are regulatory products
of another regulatory gene that are not active in the daughter cell (the bottom chromosome pair, solid square). In daughter cells, the
conditions for the next signal for division were created (hatched arrows).

cesses: the activation of genomic information, the
enhancement of cell mass, and the distribution of the
activated information in the cell mass.
3. Genetic model of ontogeny. In terms of genetics,
ontogeny combines three parallel processes: (1) an
increase in the number of functioning genetic programs
according to the increasing number of cells; (2) an
increase in the number of functioning structural genes;
and (3) a relay of activity of the regulatory ontogenetic
genes that consecutively switch on groups of structural
genes. The mutant genes found on our study belong to
the regulatory ontogenetic genes. Taking into account
the structural features and functions of these genes as
well as their special role in ontogeny, they were given a
specific name of ontogenes.
In Fig. 7, we present a genetic model of ontogeny
showing the place and role of the ontogenes in the indi-
vidual development and explaining the manifestation of
these genes. The genome of an individual consists of
structural genes and ontogenes (regulatory genes of
various ranks). An ontogene is activated by a specific
product and itself controls the product for activation of
another gene (an ontogene or a structural gene).
Although morphologically the process of ontogeny
looks like a continuous transformation of structures, the
progress of this process is controlled by ontogenes
rather than by structural genes or by the structures
themselves.
The switching of activity between the regulatory
genes occurs only during cell division. Thus, each of
the activity changes is related to a new population of
cells (at least two of them, in an extreme case), which
has different potential and different structural and func-
tional properties as compared to the original cell popu-
lation, in which the previous regulatory gene was
active.
According to the model, the regulatory genes play a
key role in ontogeny. Blocking a whole direction of
development, the mutation is likely to lead to a lethal
outcome; however, non-development of some organism
parts (legs, wings, halteres, etc.) is compatible with life,
which is indeed observed in the progeny that has mor-
phoses. A mutation may pass unnoticed if it occurred in
an inactive cis-allele, but after its activation it is mani-
fested as a lethal or a morphose. The model assumes
that the structural genes located at the ends of regula-
tory pathways may have allelic variants (trans-alleles).
Regulatory genes have only cis-alleles; alleles within
the haploid genome. Notwithstanding the structural
diploidy, the regulatory part of the genome is function-
ally haploid.
cis- AND trans-ALLELISM AS TWO GENETIC
WAYS TO GENERATE INTRASPECIFIC
VARIATION
The thesis on the existence of an invariant part of the
species genome proved to be very productive for find-
ing mutations with unusual properties. The success of
the search for these mutations is an additional argument
in favor of the idea on the existence of this genome part
[16, 17]. The results of the mutation analysis suggest
that the invariant part of the genome has a specific

RUSSIAN JOURNAL OF GENETICS Vol. 40 No. 9 2004

 FROM GENETICS OF INTRASPECIFIC DIFFERENCES 955

(a) (b)

t4

t3

t2

t1

t0

Fig. 7. Genetic model of ontogeny. (a) Genes and signaling pathways. The genome of the individual includes structural genes (small
black and hatched circles) and regulatory genes of different ranks (circles, squares, and triangles). The regulatory ontogenetic gene
is represented by a set of cis-alleles (division of the signs into sectors). t0–4, ontogeny stages. The genome is activated through a
regulated system of signal pathways (lines connecting genes; arrows). The signaling pathways are terminated by activating struc-
tural genes. Ontogeny is the process of sequential activation of regulatory genes of different ranks according to the relay principle.
Passing from the previous to the next stage of development switches off the regulatory genes functioning at the previous stage and
the structural genes responsible for presumptive structures (hatched circles). (b) Ontogeny at a late stage (t4). Switched-off genes
are shown by dotted lines. Most of the structural genes and some of the regulatory genes close to the former by the switching time
(regulatory genes of stem cells) are still active.

structure: it consists of genes, each of which is pre-
sented in several and more copies. The copies are not
identical and can be referred to as alleles. This situation is
very similar to multigene families of structural genes [35].
The alleles were more appropriately termed cis-alleles
to distinguish them from trans-alleles, that is, classical
alleles of structural genes. Ultimately, the invariant part
of the genome is also variable, but at a different level.
The introduction of the notions of cis- and trans-allel-
ism highlights, on the one hand, principal relatedness of
these two ways of generating intraspecific variation,
but, on the other hand, the existence of differences
between them.
Comparison of the two ways of generating variation
seems to be helpful for in-depth understanding of this
biological phenomenon. Here, we would like to outline
the unique features of each of them. Trans-allelism
concerns structural genes, which are located at the ends
of ontogenetic regulatory chains (Fig. 7) and thus can
change irrespective of one another. The number of
trans-alleles does not alter the size of the genome; their
quality and quantity does not affect the complexity of
the organism. We can state a priori that the level of
trans-allelic diversity would be different for different
structural genes. The structural genes that start func-
tioning early in the ontogeny, may prove to be less vari-
able or even classed as “invariant,” because slight struc-
tural defects occurring in early ontogeny may later lead
to lethality. Apparently, monomorphic genes in studies
of Altukhov and coauthors (see [16] for review) belong
to the category of structural invariant genes.
The notion of cis-allelism concerns regulatory
genes. The number of regulatory chains with participa-
tion of the given regulatory gene is at least equal to the
number of corresponding cis-alleles. A mutant impair-
ment of a cis-allele would be lethal if this allele func-
tions in the given genotype. The mortality takes the
form of dominant lethality, mainly at an early embry-
onic stage. This type of lethality, regardless of the
mutagenic factor causing it, indicates impairment of the
genetic regulatory system.
Cis-allelism should primarily be considered as a
genetic basis of individual variability. All individuals of
the same species have an identical regulatory system,
lacking broad population potential for creating diver-
sity in the form of trans-allelic polymorphism. How-
ever, the given individual can “select” a particular allele
from the cassette of cis-alleles. In view of the great
number of regulatory genes, we can expect individual
variability within the regulatory system of the species.
The only condition is non-inheritance of this choice.
Although cis- and trans-allelisms are principally simi-
lar as sources of biodiversity, they are essentially differ-

RUSSIAN JOURNAL OF GENETICS Vol. 40 No. 9 2004

956 CHADOV et al.
ent in inheritance: the former generates non-heritable
variability, whereas the latter, heritable variability.
The pattern of morphose formation in the mutants,
apart of its extreme variants, is similar to the pattern of
individual variability: morphoses are not inherited, are
asymmetric, and express only in part of the progeny.
Random combinations of cis-alleles of different
genes in regulatory chains are unlikely: in this case, the
very existence of cis-alleles as non-identical structures
loses sense. Hence, stable combinations or alleles of
different regulatory genes, and, consequently, correla-
tion between characters must exist. This sheds light on
genetic basis of character correlations. Classical genet-
ics showed its limited possibilities in explaining corre-
lation, inheritance of quantitative traits, and joint inher-
itance.
Cis-allelism of regulatory genes requires further
investigation. However, even now finding this phenom-
enon seems to open the ways for resolving the central
problem of biological evolution: the formation of a new
genome within the functioning old one [19, 25, 36].
CONCLUSIONS
The main idea of this study is that classical genetics,
notwithstanding its fundamental principles of heredity,
is but a model based only on a part of biological mate-
rial. This part encompasses characters of intraspecific
difference. Characters of intraspecific similarity consti-
tute another part of this material. The first results
obtained by studying this class of characters shows that
new principles await us. Proving these principles will
involve much research, but the available facts are suffi-
cient for their formulation. Importantly, these facts
were obtained on the same genetic field (hybrid analy-
sis) as forms the basis of classical genetics. This means
that they can be tested using the already verified crite-
ria.
An important genetic generalization that can be for-
mulated even now states that in the process of intraspe-
cific hybridization, the individuals exchange mainly
identical genetic information related to the organization
of ontogeny. The origin of this information dates back
virtually to the first steps of the appearance of the living
matter. This information increases in evolution of living
organisms. It does not have allelic variants in the com-
monly accepted sense of the term. The invariant part of
the genome controls the program of individual develop-
ment, namely, its regulatory part. New viable variants
of this program appear in the process of evolution.
These variants reliably persist as species programs.
The principle of population polymorphism based on
the Mendelian approach cannot be regarded as a gen-
eral genetic principle valid for all genes without excep-
tion. Apparently, some structural genes controlling
“ancient” functions also fall under the category of
monomorphic. Examples of monomorphism have been
known since the early 1970s [16]. However, the mech-
RUSSIAN JOURNAL OF GENETICS
anism of entering the invariant genome part and the
mechanism of maintaining monomorphism seems to be
different for this gene group.
The assumption of an invariant part of the genome
may seem illogical, but only at the first glance. Invari-
ability at the diploid genomic level is atoned by the exist-
ence of cis-allelism, that is, variability at the haploid
genomic level. Cis-allelism brings us to the resolution of
the issue of individual “nonheritable” variability.
The principle stating that “where is a character,
there is a gene,” which underlies classical genetics, is
not related to genetics in general. The regulatory sys-
tem controlling development cannot operate according
to this principle. The product produced by a regulatory
ontogenetic gene cannot function at the location of this
gene (in the same cell). The cell must undergo division,
which would result into the product functioning in the
daughter cells, in which the “old” gene is inactive. Only
after that will the product activate a new regulatory
gene. This is the only possibly way of “quantization” of
the developmental implementation of genetic informa-
tion. The presence of the product with the switched-off
gene is in essence the “presence of the character with-
out the gene.” This seems to be a rule in ontogeny. Sec-
tions “Maternal Effect” and “Paternal Effect” list illus-
trative examples of the presence of a character (mor-
phose) in an individual without the presence in this
individual of the mutant chromosome causing the mor-
phoses.
The principle of obligatory activity of both homolo-
gous genes in a diploid individual also is not a general
genetic rule. Ontogenetic genes are characterized by
allelic exclusion.
Activity of each gene in each member of the species
is either not a general genetic principle. It does not hold
for cis-alleles of regulatory genes. The individual
genomes must be filled with genetic structures that did
not show activity during the lifetime of this particular
individual. Since each living organism inevitably
passes through ontogeny, and regulatory ontogenetic
genes are characterized by maternal and paternal
effects, the latter must often accompany inheritance of
characters. Thus, it is clear that genetics of intraspecific
similarity shows uniqueness even at this early stage of
its history.
The understanding of the fact that, owing to its
approach, classical genetics did not and could not pro-
vide a complete description of inheritance and func-
tioning of all genetic material, would lead to critical
revision of the research directions that did not yield
substantial results during the long history of research
based on the classical ideology. This primarily con-
cerns studies of evolution based on population poly-
morphism and selection of allelic variants. The errone-
ous nature of this approach was pointed out as early as
in the 1970s [10, 11]. The cis-allelic organization of the
regulatory genomic part opens avenues for developing
the ideas of evolution based on duplications [37–39],
Vol. 40 No. 9 2004
 FROM GENETICS OF INTRASPECIFIC DIFFERENCES
and in a different, more natural, variant: “duplications”
exist in any genome, their number being no less than
the number of cis-alleles of regulatory ontogenetic
genes [25]. The first “gift” presented by genetics of
intraspecific similarity to the evolution theory is the
relationship between the activity of regulatory gene
alleles and the presence of chromosomal rearrange-
ments in the genome [19]. The problem of the role of
chromosome rearrangements in speciation may be
resolved.
Considering problems of ontogeny, we should not
overlook the fact that the gene activity that changes
depending on the stage of development concerns genes
of different categories. These may be structural genes
controlling the formation of presumptive structures and
presumptive functions, and regulatory genes. The
former can be detected and studied by classical meth-
ods but the latter cannot.
As to quantitative characters, they are integral char-
acteristics of characters of intraspecific similarity.
Hence, their description requires analysis of a multi-
level regulatory system controlling development. The
knowledge of this system is scarce. If this system con-
sisted only of a great number of structural genes, the
problem would have long been resolved.
There is a set of terms denoting characters that can
be analyzed by classical genetic methods. These char-
acters are called simple, monogenic, Mendelian, quali-
tative, alternative, having good inheritance. However,
they would be more aptly termed heritable characters
of intraspecific difference. This class include traits
appearing at the change of one allele of a structural
gene for another. Some of them result from a change in
several structural genes (epistasis). The proposed term
contains all the above definitions and, most impor-
tantly, links genetic concepts and their biological mean-
ing.
Classical gene analysis leaves out non-heritable
(individual) characters of intraspecific difference and
all characters of intraspecific similarity. In spite of their
different names, these character classes are related. The
former demonstrate admissible regulation changes,
which do not result in a breakdown of the biological
system. The latter are characteristics of the breakdown
having already occurred, of an appearance of a new sys-
tem incompatible with the old one. The possibility for
studying the both classes is open. The present study,
however, was focused on the possibilities of direct
genetics. A broader consideration of characters of
intraspecific similarity and “the character in general”
will be presented elsewhere.
As stated in Introduction, the category of intraspe-
cific similarity characters has a complex structure. This
category includes traits that formed in organisms dur-
ing the long history of evolution of the living matter.
Until the present, the information on genetic material
responsible of characters of superspecies level was
expected to be obtained only by manipulation with
RUSSIAN JOURNAL OF GENETICS Vol. 40 No. 9
957
DNA as the hereditary substance (intraspecific DNA
hybridization, comparison of genetic texts in members
of different taxa). The approach outlined in this study
opens a possibility to obtain such information in tradi-
tional hybrid analysis of members of the same species.
Importantly, this approach can be used to trace pro-
cesses occurring in generations.
ACKNOWLEDGMENTS
We thank Yu.P. Altukhov for discussion and many
valuable critical comments on the results.
This work was supported by the Russian Foundation
for Basic Research, grant no. 01-04-48899.
REFERENCES
1. Kondakov, N.I., Logicheskii slovar’–spravochnik (Logi-
cal Dictionary–Handbook), Moscow: Nauka, 1975.
2. Gaisinovich, A.E., Zarozhdenie i razvitie genetiki (The
Origin and Development of Genetics), Moscow: Nauka,
1988.
3. Timiryazev, K.A., Sochineniya (Works), Moscow:
Sel’khozgiz, 1937–1939, vols. 2, 5–7.
4. Filipchenko, Yu.A., Evolyutsionnaya ideya v biologii
(The Evolutionary Idea in Biology), Moscow: Izd-vo
Sobashnikovykh, 1923.
5. Filipchenko, Yu.A., Izmenchivost’ i metody ee izucheniya
(Variation and Methods to Study It), Leningrad: Gosiz-
dat, 1929, 4th ed.
6. Gershenzon, S.M., Osnovy sovremennoi genetiki (Basics
of Modern Genetics), Kiev: Naukova Dumka, 1983,
p. 220.
7. Rieger, R. and Michaelis, A., Geneticheskii i tsitogenet-
icheskii slovar’ (Genetic and Cytogenetic Dictionary),
Moscow: Kolos, 1967.
8. Singer, M. and Berg, P., Genes & Genomes: A Changing
Perspective, Mill Valley, California: Univ. Sci. Books,
1991, vol. 2.
9. Altukhov, Yu.P., On the Relationship of Monomorphism
and Polymorphism of Hemoglobins in Fish Microevolu-
tion, Dokl. Akad. Nauk SSSR, 1969, vol. 189, no. 5,
pp. 115–117.
10. Altukhov, Yu.P. and Rychkov, Yu.G., Population Sys-
tems and Their Structural Components: Genetic Stability
and Variation, Zh. Obshch. Biol., 1970, vol. 31, no. 5,
pp. 507–526.
11. Altukhov, Yu.P. and Rychkov, Yu.G., Genetic Monomor-
phism of Species and Its Possible Biological Signifi-
cance, Zh. Obshch. Biol., 1972, vol. 33, no. 3, pp. 281–
300.
12. Diver, C., Fossil Records in Mendelian Mutants, Nature,
1929, vol. 124, p. 183.
13. Rychkov, Yu.G. and Movsesyan, A.A., Genetic Anthro-
pological Analysis of the Distribution of Cranial Abnor-
malities in Siberian Mongoloids in Connection with
Their Origin, Byull. Mosk. O–va Ispyt. Prir., Otd. Biol.,
1972, vol. 43, pp. 114–132.
2004
958 CHADOV et al.
14. Movsesyan, A.A., Some Aspects of the Genetics of
Modern and Ancient Populations of Siberia, Vopr.
Antropol., 1973, no. 45, pp. 77–84.
15. Altukhov, Yu.P. and Kalabushkin, B.A., Stable Polymor-
phism in Modern and Fossil Populations of Mollusk Lit-
torina squalida, Dokl. Akad. Nauk SSSR, 1974, vol. 215,
no. 6, pp. 1477–1480.
16. Altukhov, Yu.P., Geneticheskie protsessy v populyatsi-
yakh (Genetic Processes in Populations), Moscow:
Nauka, 1989.
17. Altukhov, Yu.P., Species and Speciation, Soros. Obrazo-
vat. Zh., 1997, no. 4, pp. 2–10.
18. Altukhov, Yu.P. and Abramova, A.B., Species-Specific
Random Amplified Monomorphic DNA, Russ. J. Genet.,
2000, vol. 36, no. 12, pp. 1411–1417.
19. Chadov, B.F., Mutations Able to Initiate Speciation,
Evolyutsionnaya biologiya: Materialy konferentsii
“Problema vida i vidoobrazovanie” (Evolutionary Biol-
ogy: Proc. Conf. “The Problem of Species and Specia-
tion”), Stegnii, V.N., Ed., Tomsk: Tomsk. Gos. Univ.,
2001, vol. 1, pp. 138–162.
20. Ashburner, M., Drosophila: A Laboratory Handbook,
Cold Spring Harbor, New York: Cold Spring Harbor
Lab., 1989.
21. Chadov, B.F., Chadova, E.V., Kopyl, S.A., and Fedoro-
va, N.B., A New Class of Mutations in Drosophila mel-
anogaster, Dokl. Akad. Nauk, 2000, vol. 373, no. 5,
pp. 714–717.
22. Chadov, B.F., Mutations in the Regulatory Genes of
Drosophila melanogaster, Proc. Int. Conf. Biodiversity
and Dynamics of Ecosystems in North Eurasia, Novosi-
birsk, August 21–26, 2000, Novosibirsk: Inst. Tsitol.
Genet., 2000, pp. 16–18.
23. Chadov, B.F., Chadova, E.V., Kopyl, S.A., and Fedo-
rova, N.B., Delayed Activation of the Maternal Genome
in Early Drosophila Development, Dokl. Akad. Nauk,
2001, vol. 378, no. 6, pp. 841–845.
24. Chadov, B.F., “The Image” of the Regulatory Gene in
Experiments with Drosophila, Russ. J. Genet., 2002,
vol. 38, no. 7, pp. 725–734.
25. Chadov, B.F., Facultative Dominant Lethals: Genetics,
Ontogeny, and Phylogeny, Evolyutsionnaya biologiya:
Materialy II konferentsii “Problema vida i vidoobrazo-
RUSSIAN JOURNAL OF GENETICS
vanie” (Evolutionary Biology: Proc. II Conf. “The Prob-
lem of Species and Speciation”), Stegnii, V.N., Ed.,
Tomsk: Tomsk. Gos. Univ., 2002, vol. 2, pp. 118–142.
26. Bridges, C.B., Non-Disjunction as Proof of the Chromo-
some Theory of Heredity, Genetics, 1916, vol. 1, pp. 1–52,
107–163.
27. Lewin, B., Genes, New York: Wiley, 1983.
28. Frizen, G., Roentgenomorphoses in Drosophila, Biol.
Zh., 1935, vol. 4, no. 4, pp. 687–704.
29. Rapoport, I.A., Specific Morphoses Induced by Chemi-
cal Compounds in Drosophila melanogaster, Byull.
Eksp. Biol. Med., 1939, no. 7, pp. 415–417.
30. Goldschmidt, R., Theoretical Genetics, Berkeley: Univ.
California Press, 1957.
31. Goldschmidt, R. and Piternick, L., The Genetic Back-
ground of Chemically Induced Phenocopies in Droso-
phila, J. Exp. Zool., 1957, vol. 135, pp. 127–202.
32. Goldschmidt, R. and Piternick, L., The Genetic Back-
ground of Chemically Induced Phenocopies in Droso-
phila, J. Exp. Zool., 1957, vol. 136, pp. 201–228.
33. Korochkin, L.I., Vvedenie v genetiku razvitiya (Introduc-
tion to Developmental Genetics), Moscow: Nauka,
1999.
34. Chadov, B.F. and Fedorova, N.B., An Elementary Event
of Ontogeny, Dokl. Akad. Nauk, 2003, vol. 389, no. 3,
pp. 408–412.
35. Hood, L., Cambell, J.H., and Elgin, S.C.R., The Organi-
zation, Expression, and Evolution of Antibody Genes
and Other Multigene Families, Annu. Rev. Genet., 1975,
vol. 9, pp. 305–353.
36. Carson, A., The Genetics of Speciation at the Diploid
Level, Am. Nat., 1975, vol. 109, pp. 83–95.
37. Serebrovsky, A.S., The scute and achaete Genes of
Drosophila melanogaster and a Hypothesis of Their
Divergence, Dokl. Akad. Nauk SSSR, 1938, vol. 19,
nos. 1–2, pp. 77–81.
38. Ohno, S., Geneticheskie mekhanizmy progressivnoi
evolyutsii (Genetic Mechanisms of Progressive Evolu-
tion), Moscow: Mir, 1973.
39. Khesin, R.B., Nepostoyanstvo genoma (Genome Incon-
stancy), Moscow: Nauka, 1984.
Vol. 40 No. 9 2004