Journal of Biotechnology

and Crop Science

6(8): 44-52, 2017

New quantitative trait loci (QTLs) for turcicum leaf

blight in maize
Rajesh Singh, RP Srivastava
Received: 16 April 2017 Revised Accepted: 18 June 2017

ABSTRACT
Turcicum Leaf Blight (TLB) is an important maize disease which causes heavy loss every year. A study was conducted to
identify quantitative trait loci (QTLs) for NCLB resistance in maize. A mapping population from F 2:3 families were
developed involving the two inbred lines viz., CM 212 (susceptible) and CM 338 (resistant) and evaluated in two Indian
environments (Varanasi, Uttar Pradesh and Nagenahalli, Karnataka) to locate and map QTLs. Data on four disease
severity traits viz., Percent Disease Index (PDI), Area under Disease Progress Curve (AUDPC-PDI) based on PDI, Lesion
Area (LA), AUDPC based on lesion area (AUDPC-LA) were generated for QTL mapping. Four QTLs were identified on
4th chromosome of maize.

Key Words: Area Under Diseases Progress Curve (AUDPC), Percent Diseases Index (PDI), Quantitative
Trait Loci (QTL), Turcicum leaf blight (TCLB)

Turcicum Leaf Blight (TLB) is caused by the
ascomycete fungus Setosphaeria turcica (Luttrell)
Leonard and Suggs, with its conditional state
Exserohilum turcicum, (Passerini) Leonard and
Suggs (Renfro & Ullstrup, 1976). This disease
depends on the level of genetic resistance of the
genotype, climatic conditions during the growth
cycle and the production system and causes
significant losses to yield and grain quality the
disease symptoms primarily appear on the leaves.
Plants may be infected at any growth stage, but
usually at or after anthesis. Lesions on susceptible
plants are 4-20 cm long and 1-5 cm wide, which is
elliptical in shape and grayish-green to tan in color.
Severity of TLB increases exponentially at highly
humid and low temperature conditions (Singh et al
2004) at certain places heavy dew has also being
cited as one of the factors that increase TLB
severity. Screening of molecular markers for
Rajesh Singh ( )
Department of GPB, IAS, BHU, Varanasi -221005
Email: rsingh6361@gmail.com
RP Srivastava
Department of Agriculture, Quantum Global Campus,
Mandawar, Roorkee, Dehradun-247167
parental polymorphism among the maize cultivars
forms the basis for constructing high-density genetic
linkage map that can facilitate Quantitative Trait
Loci (QTL) mapping against TLB. QTL
identification in return helps in marker assisted
selection (MAS) process for improving genetic traits
in crop plants. Not much work had been done in the
Indian germplasms for precise identification of
QTLs against TLB. Only few QTLs conferring
resistance to pathogens had been validated (Abalo et
al 2009, Asea et al 2009, 2010). It is therefore
important to document the reproducibility of
candidate rQTLs in a specific population by
targeting the environment of interest before
considering the population for selection (Asea et al
2010). The aims of the present study were aimed to
identify new QTLs TLB in maize.
Plant Material: Maize inbred CM 212 derived from
population A-Theo 21 after 6-7 generation of
inbreeding, is early duration maize inbred with high
susceptibility to NCLB and known for its good
combining ability and developing single crosses
with high heterosis. The male parent (CM 338) was
derived from the maize population of Almora which

44

is a highly TLB resistant line in early maturity
group. The F2:3 families of selfed plants of CM 212
CM 338 were raised and evaluated through field
trials for resistance against NCLB in two NCLB
environments viz., Agriculture Research Farm,
Banaras Hindu University, Varanasi, Uttar Pradesh,
India (Varanasi-E1) and NCLB Hot spot at Zonal
Agriculture Research Station, Nagenahalli, Mandya,
Karnataka, India (Nagenhalli-E2). For pollination,
individual flowers of the selected female parent were
hand emasculated and pollinated with the pollen dust
from the male parent in the cool hours of the day to
get sufficient F1 seeds. F1s plants were selfed to
produce F2 seeds by covering with a pollen bag to
prevent out crossing from other breeding material.
F2s plants were selfed to raise F2:3 mapping
population and seeds of each F2:3 families were
increased by single seed decent method for TLB
evaluation.
Disease development: The spreader-row technique
was used for field inoculation of a susceptible check
(Dhiari local) for Varanasi that was planted every
20th rows to promote disease build up and spread.
Inoculums were produced and maintained separately
on susceptible varieties. Plants were inoculated at 6
7 leaf stages. The inoculums were prepared by
growing the fungal mycelium on sorghum grains.
After proper fungal growth (7-10 days), the grains
were dried in shade at room temperature. A fine
powder of these grains was prepared with the help of
a mixergrinder and a pinch of this powder was put
in the leaf whorl. Inoculation was done in evening to
avoid the maximum day temperature during
incubation period. The procedure was same as
reported by Carson et al (2004). In Nagenahalli the
isolate of pathogen was provided by the Zonal
Agriculture Research Station, Nagenahalli. The
lactose casein hydro-lysate agar medium was used to
produce conidia. Inoculums were prepared,
multiplied, washed from plates into a container for
J of Biotech & Crop Sci (2017) 6(8): 46-52
preparation of suspension. Plants were inoculated at
5-7 leaf stage by pouring 1 ml of inoculums on leaf
whorl.
Disease Assessments: Four disease traits of NCLB
viz., Percentage Disease Index (PDI), Area Under
Disease Progress Curve based on PDI (AUDPC-
PDI), Lesion area (LA) and Area Under Disease
Progress Curve based on Lesion area (AUDPC-LA),
were recorded in two different environments (E1 and
E2). AUDPC was estimated using the formula given
by Campbell and Madden (1991):
Where Xi is the disease index expressed as a
proportion at the ith observation, ti is the time (days
after planting) at the ith observations and n is the
total number of observations. AUDPC-PDI and
AUDPC-LA were also calculated at the same growth
stages in the two environments.
Statistical Analysis: Statistical analysis of all four
characters [PDI, AUDPC (PDI), Lesion Area and
AUDPC (LA)] for ANOVA and traits correlation
was performed by PROC GLM procedure using
SAS (V 9.2) software package (SAS Institute Inc.,
2004). ANOVA was calculated for all four disease
parameters in each environment as well as
combined/ pooled over environment using SAS (V
9.2) software package (SAS Institute Inc., 2004).
Map construction and QTL detection: Linkage map
was constructed using SSR primers identified as
polymorphic during the parental polymorphism
survey. For each segregating marker, a Chi-square
analysis {2= (Observed-Expected)/ Expected} was
performed to test for deviation from the expected
segregation ratio (1:2:1). Linkage analysis of SSR
markers was conducted using the Kosambi (1944)
mapping function with a minimum log10 odds ratio
(LOD) of 2.0 and maximum recombination
45
J of Biotech & Crop Sci (2017) 6(8): 44-52

Figure 1 DNA amplified products of bnlg 2190, bnlg 1112, umc 1051 and umc 1064 , bnlg 1208 and phi 019 of 8 maize inbred
lines ( CM 104, CM 105, CM 118, CM 126, CM 145, CM212, V 336, V338) for parental polymorphism survey for Northern Corn
Leaf Blight in Maize.

frequency of 0.4 performed by Map-Maker/EXP 3.0
(Lander et al 1987). Quantitative trait loci (QTL)
analysis for each individual environment and a
combined one, across all environments were
performed by composite interval mapping using
Windows QTL Cartographer 2.5 (Basten et al 2002).
A QTL was considered significant when the LOD
(log10 of the likelihood of odds ratio) value that
derived from permutation analysis was large than 2.
Additive and dominance effects for detected QTLs
were estimated using the Zmap QTL procedure of
QTL Cartographer. The R2 value, the percentage of
the phenotypic variance explained by marker
genotype at the QTL, (coefficient of de termination)
was taken from the peak QTL position as estimated
by QTL Cartographer. Gene action was determined
by the ratio of the absolute value of the estimated
dominance effect divided by the absolute value of
the estimated additive effect (d)/(a) following Stuber
et al (1987); (additive = 0 to 0.20; partial dominance
= 0.21 to 0.80; dominance = 0.81 to 1.20; and over
dominance > 1.20).
QTL mapping facilitates studies on interactions
between resistance genes, pathogens and
environment. In the present study we are reporting 2
TLB resistant QTLs in maize in India. Moderate to
high incidence of disease for all the 4 traits (PDI,

46

AUDPC-PDI, LA, and AUDPC-LA) was observed
in both the environments E1 and E2. However, the
disease incidence was high in E2 compared to E1
despite similar artificial epiphytotic conditions were
provided in both the environments. Nagenahalli (E2)
is considered as Hot Spot for TLB in India. High
natural incidence of TLB in E2 was also reported
earlier by several earlier workers in E2 compared to
rest of the country (Carson et al 2002, Singh et al
2004, Pandurange Gowda et al 2012,
Chandrashekara et al 2014, Singh et al 2014). In the
present study both environments E1 and E2 had
adequate level of humidity. In E1 (Varanasi) during
July although the humidity remains high but average
temperature ranges between 32-35 OC that does not
favor natural incidence of the disease. Whereas in
E2 (Nagenahalli) the average temperature remains
around 20-25 OC, which is quite optimal for TLB.
Balint-Kurti et al (2010) also mapped QTLs for TLB
in two environments viz, in Clayton (NC) and
Aurora (NY). They observed that diseases pressure
was lower in Clayton (NC) than in Aurora (NY).
They explained that it was because of slightly high
temperature during the growing season (the average
maximum temperature during July was 32 OC) in
Clayton (NC), while in Aurora (NY), the cooler
temperatures (average maximum for July was 25 OC)
were optimal temperature for TLB. They also used
different inoculation methods in the two
environments. So, the trend in the present study
supports adoption of different inoculation techniques
owing to local practices for creating artificial
epiphytotic conditions for NCLB.
Among the four traits studied for evaluation of F 2:3
lines in two environments indicated that the traits
PDI and AUDPC-PDI responded better to disease
severity particularly in E2 than E1. The disease
progress curve was just near or above susceptible
check curve in disease severity for PDI (Fig. 2)
whereas the average of lines of E2 population was
above the susceptible check in case of AUDPC-PDI.
On the other hand for Lesion Area the progress
curve indicated mean F2:3 lines were falling
J of Biotech & Crop Sci (2017) 6(8): 44-52
somewhere between resistance and susceptible lines.
Mapping of QTLs in the current study has also been
done in F2:3 populations as have been suggested that
it has several intrinsic advantages for QTL mapping
(Rodier et al 1995, Smith and Kinsey 1993, Welz et
al 1998, 1999a, 1999b, 2000, Roder et al 1998,
Davis et al 1999, Schechert et al 1999, Temnykh et
al 2000). The heavy disease pressure maintained in
field plots with artificial epiphytotic condition
combined with replicated disease evaluations in two
different environments ensured that our assay was
sufficiently sensitive to detect all QTL effects on
NCLB resistance in F2:3 populations. Due to
environmental variations in two environments we
chose to analyze each environment with respect to
disease traits separately as well as pooled analysis
over environments. We initially observed four
QTLs, all located on Chromosome arm 4. All the
tow QTLs identified were effective (R2>50%) and
were environment-specific (Table-5). Out of 4
disease traits evaluated in two environments only
PDI helped in identification of two QTLs. Balient-
Kurti et al (2010) also reported many QTLs for
NCLB resistance, out of which 6 were present on
Chromosome arm 4 at bin locations viz., 4.08 (Trait
BLUPWMD with flanking markers isu053a-
isu144a), 4.07-4.08 (Trait AU06WMD with flanking
markers asg33-umc1667), 4.07-4.08 (Trait
AU07WMD with flanking markers asg33-ufg23),
4.07-4.08 (Trait CL07WMD with flanking markers
umc1775-mmp3), 4.06 (Trait AU06IP with flanking
markers umc2027-zm1) and 4.07-4.08 (Trait
BLUPDTA with flanking markers umc52-
php10025). The two QTLs were present on 4th
chromosome somewhere between bin locations 4.05
to 4.08, where all the six QTLs reported by Balint-
Kurti et al (2010) are present. They reported these
QTLs from the mapping population of B73
(susceptible) x Mo17 (resistant) in the three
environments Clayton, NC in 2007 (CL07), Aurora,
NY in 2007 (AU07) and Aurora, NY in 2006
(AU06) with the help of 3 traits, viz., WMD, IP and
DTA (Days to Anthesis). The difference, they
reported for disease trait WMD with moderate effect
47
 J of Biotech & Crop Sci (2017) 6(8): 44-52

(R2<10%). We are reporting it a significant QTL
with 50.2 to 53.0 % phenotypic variation. Other
QTLs (2 & 4) were environment specific as reported
by Welz et al (1999a) who identified an
environment-specific NCLB resistant QTL derived
from the maize lines Lo 951 CML 202.
Environment specific NCLB resistant QTLs have
been observed in a number of previous studies
(Brown et al 2001, Jiay et al 1999, Welz et al 1999a,
Albeno et al 2009, Balint-Kurti 2008, 2010, Asea et
al 2009, 2012). Recently, Balint-Kurti et al (2010)
used Intermated B73 x Mo17 (IBM) population and
evaluated in three environments for three traits
related to TLB resistance, WMD, IP, and DTA. Two
WMD QTLs were detected in bins 2.00/2.01 and
4.08 from the overall analysis and between the two
the QTL in bin 4.08 was the only one detected in all
three environments analyzed separately. Likewise,
only one IP QTL in bin 2.02 was detected in all three
environments and from the overall analysis. In our
study, two QTLs for PDI was detected in bins
4.03/4.05 and 4.08/4.1 in the two environments
analyzed separately. Another two QTLs were also
detected on the same chromosome 4, one (QTL1) at
marker interval bnlg 1126-bnlg 1159 in bin location
4.03/4.05 with 80 cM map position with highest
LOD value 4.85 and R2 value 52.7 and the other
QTL (QTL3) was detected in the combined AUDPC
at bin location 4/4.07 with marker interval bnlg
1927-umc 1008 with 40 cM map position. In maize,
resistance to TLB is a complex quantitatively
inherited trait (Juliana et al 2005, Kumar et al 2011).
Comparison of the QTL locations with a previous
study indicated some consistency based on bin
positions. Brown et al (2001) analyzed F2:3
populations derived from sweet corn lines IL731 and
W6786 in two different environments. They
identified 33 regions in the maize genome were
associated with partial Resistance describing from
5.9 to 18% of the total phenotypic variability. Of six
regions common in both years, three were associated
with partial resistance to Stewarts wilt
(chromosomes 4:07, 5:03 and 6:04), one was
associated with TLB (chromosome 9:05), and two
were associated with common rust (chromosomes
2:04 and 3:04). They also identified two QTL
associated with anthocyanin production on
chromosomes 10:6 and 5:03. QTL for

Table 1 Mean value of NCLB AUDPC, PDI, lesion area, AUDPC based on Lesion area and coefficients of variation for
175 F2:3 families from the cross of CM 212 CM 338 from individual environments and across environments.
Percent disease index AUDPC (PDI) Lesion Area AUDPC (Lesion Area)
(PDI)
Genotype E1* E2** Pooled E1* E2** Pooled E1* E2** Pooled E1* E2** Pooled
CM 212 54.27 85.25 71.15 1320.20 3002.80 2088.42 14.25 28.65 20.45 273.30 740.90 515.15
CM 338 27.25 41.65 36.25 798.55 1920.11 1360.45 4.55 6.85 5.65 121.45 164.37 147.25
F2:3 mean 36.25 72.85 54.22 975.41 2785.51 1856.55 10.95 25.47 16.40 217.55 328.25 310.85
CV# 6.25 3.45 6.95 5.80 4.70 6.45 3.25 2.05 2.43 3.25 3.16 3.25
# CV was estimated from 159 entries including parents in RBD; *Agricultural Research Farm, BHU, Varanasi Kharif 2012; ** Zonal
Agricultural Research Farm, Mandya, Karnataka Kharif 2012.

Table 2 Heritability of four disease traits (Percent Disease Index, AUDPC Area under Disease Progress Curve, Lesion
Area and AUDPC (Lesion area) involving 159 F2:3 families with parents over the environments.
Characters Heritability
PDI 0.56
AUDPC (PDI) 0.48
LA 0.99
AUDPC (LA) 0.99

48

Table 3 QTL identified for Percent disease index (PDI) and Area under disease progress curve in F2:3 populations of
cross CM 212 CM 145.
QTLs Trait Bin Marker- Map Position
Interval
QTL 1 PDI 4.01/4.05 bnlg1126 -
bnlg1159
QTL 2 PDI 4.08/4.1 umc1051-
bnlg1917
NCLB from this study and other studies were
compared to disease resistance loci reported by
Dingerdissen et al (1996) and Welz and Geiger
(2000). They reported AUDPC is more appropriate
trait for QTL study in maize. Dingerdissen et al
(1996) identified QTLs for AUDPC on chromosome
1 and on 2S, 3L, 5S, 6L, 7L, 8L and 9s but QTL on
chromosomes 3L, 5S, 7L and 8L were found
significant across environments whereas, Welz and
Geiger (2000) discovered QTL for AUDPC were
located on chromosome 1 to 9 in three different
mapping populations. All three populations carried
QTL in identical genomic regions on chromosomes
viz., Chromosome-3 (bin 3.06/07), chromosome-5
(bin 5.04) and chromosome 8 (bin8.05/06). In our
study QTL for AUDPC has been identified in 4/4.07
with 56.2% phenotypic variance in individual
environment. Gene action was mostly partially
dominant or recessive. Generation means analyses
with Mo17 (Carson, 1995) and other germplasm
(Hughes, 1971) suggested that additive gene action
prevailed and that the size of non-additive effects
varied among populations and between years. In our
study gene action was over dominance for all the
regions that were identified. This result is
accordance to Souza et al (2008), who observed over
dominance gene action for mostly region for SCMV
disease in maize.
One of the major goals of QTL mapping is to locate
markers that can be broadly used for MAS in a
breeding program. One major concern against using
MAS has been the lack of consistency of QTLs
across environments. In the present investigation,
four QTLs identified were found significant in the
single environment. It might be Genotype x
Environment interaction or low disease appearance
J of Biotech & Crop Sci (2017) 6(8): 44-52
LOD R2 Gene effects Gene
(cM) D A d/a action
70.0 4.80 50.0 11.20 4.60 2.20 OD
50.0 2.72 55.0 -5.06 2.75 - 1.75 OD
of first environment. This result is similar to
Freymark et al (1993, 1994) who tested the
population in 1991 at one location in Iowa, USA
under low disease severity. The population was also
genotyped at 112 RFLP loci to compare the
effectiveness of resistance QTL in temperate vs.
tropical environments. We therefore report 2 QTLs
involving diseases trait PDI on chromosome 4 at the
NCLB hot spot Nagenahalli (E2) and suggests that
the same location might be used for the transfer of
resistance alleles to susceptible lines. It would also
be helpful to initiate pyramiding program for
multiple genes by MAS that may control different
mechanisms of resistance.
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