Exploring the Genetic Basis of Northern Leaf Blight via Genome Wide Association Mapping in Maize.pdf

1、Gigantic efforts are required from the scientific community to find out genuine sources ofresistance and overcome the most abstruse phenomenon of disease resistance.Maize being thethird largest staple in the world is aff

2、ected by more than 100 pathogens.With the advent ofmolecular markers especially the single nucleotide polymorphism (SNP), the process of fullgenome screening has become easier and the scientists are trying to unleash the

3、 hidden truth ofdisease resistance.We performed meta-analysis for northern leaf blight (NLB), southern leafblight (SLB), and gray leaf spot (GLS), with the aim to find out the total number of QTL anddepict some real QTL

4、for molecular breeding and marker assisted selection (MAS).Our analysisrevealed that disease resistance QTL was randomly distributed in maize genome.63 QTL werecontrolling more than one disease revealing the presence of

5、multiple disease resistance (MDR).
　　44 real-QTL were observed based on 4 QTL as a standard in specific region of genome duringthis analysis.Minimum confidence interval (CI) was observed for a QTL on chromosome three,

6、while on chromosome 8 two nucleotide binding site (NBS) genes in one QTL were observed.Wealso confirmed the Ht1 and Ht2 genes within the region of real QTL.On chromosome 3, weobserved several cluster and maximum MDR QTL

7、indicating that the apparent clustering couldbe due to genes exhibiting pleiotropie effect.The biggest cluster was found on chromosome 5and significant relationship was observed between the number of disease QTL and tota

8、l genesper chromosome based on the reference genome B73.Therefore, we concluded that diseaseresistance genes are abundant in maize genome and these results can unleash the phenomenon ofMDR.
　　We evaluated the most div

9、erse maize population including 999 individuals forquantitative resistance under the epiphytotic of Exserohilum turcicum across severalenvironments using SNP markers.High-resolution genome-wide association analysis wasco

10、nducted using 56110 SNP markers, which were evenly distributed throughout the genome.Weobserved that these markers controlled 42.2, 47.4, and 53.8 ％ of the total genetic variance forarea under disease progress curve (AUD

11、PC), mean rating and maximum rating, respectively.SNP based genome wide association mapping revealed a total of 49 significant loci for thesetraits, among which 4 genes were common for all the three traits.Haplotype base

12、d associationmapping revealed six and seven alleles for AUDPC and maximum rating, while five alleles weredetected for mean rating.Among these, four alleles were common for the three traits, which werelocated on chromosom

13、es 7, 8 and 10.The results for Anderson-Darling (A-D) test revealed morethan 100 candidate loci in sub-group A while sub-group C and B harbored few or even no genesfor different traits explaining the differences in the g

14、enetic background of the germplasm in eachsub-group.The possible candidate genes are GRMZM2G171605, GRMZM2G100107,GRMZM2G158141 and GRMZM2G020254.Among these genes the GRMZM2G100107 wasconfirmed for all the three traits

15、using SNP and haplotype based association mapping andconfirmed by A-D test as well.The other gene (GRMZM2G020254) was detected for two traitsin SNP based analysis while significant for three traits in haplotype based ana

16、lysis.Some of thegenes were adjacent to already known possible candidate genes that allow more investigation asputative causal genes underlying quantitative disease-resistance QTL.
　　Another study was conducted to con

17、firm some loci in maize genome for SLB usinglinkage mapping in a RIL population (Yu87-1/Zong 3).The analysis of variance showed highlysignificant differences in the germplasm and high broad-sense heritability (0.76) was

18、observedfor SLB resistance.An integrated genetic linkage map was constructed using 13759 SNPmarkers, spanning a total of 2710 cM of the maize genome with an average interval of 0.2 eM.Three QTL for resistance to SLB were

19、 identified by CIM, which reside on chromosome 3, 5, and7, together accounting for 7.27 to 14.40％ of the phenotypic variation for this trait.Two of theseQTL were contributed by the resistant parent 87-1 (Chr 3 and 5) and

20、 overall the additive QTLexplained 30.29％ of the total phenotypic variation.Therefore, we concluded that NLB and SLBare very complex traits no single major gene is responsible for resistance while several minorgenes cont