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利用 SSR 标记进行热带玉米褐斑病抗性的群体结构分析和关联作图。

Population Structure Analysis and Association Mapping for Turcicum Leaf Blight Resistance in Tropical Maize Using SSR Markers.

机构信息

ICAR-Indian Institute of Maize Research, Ludhiana 141004, India.

Dryland Agriculture Research Station, SKUAST-K, Srinagar 190001, India.

出版信息

Genes (Basel). 2022 Mar 29;13(4):618. doi: 10.3390/genes13040618.

DOI:10.3390/genes13040618
PMID:35456424
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9030036/
Abstract

Maize is an important cereal crop in the world for feed, food, fodder, and raw materials of industries. Turcicum leaf blight (TLB) is a major foliar disease that can cause more than 50% yield losses in maize. Considering this, the molecular diversity, population structure, and genome-wide association study (GWAS) for TLB resistance were studied in 288 diverse inbred lines genotyped using 89 polymorphic simple sequence repeats (SSR) markers. These lines werescreened for TLB disease at two hot-spot locations under artificially inoculated conditions. The average percent disease incidence (PDI) calculated for each genotype ranged from 17 (UMI 1201) to 78% (IML 12-22) with an overall mean of 40%. The numbers of alleles detected at a locus ranged from twoto nine, with a total of 388 alleles. The polymorphic information content (PIC) of each marker ranged between 0.04 and 0.86. Out of 89 markers, 47 markers were highly polymorphic (PIC ≥ 0.60). This indicated that the SSR markers used were very informative and suitable for genetic diversity, population structure, and marker-trait association studies.The overall observed homozygosity for highly polymorphic markers was 0.98, which indicated that lines used were genetically pure. Neighbor-joining clustering, factorial analysis, and population structure studies clustered the 288 lines into 3-5 groups. The patterns of grouping were in agreement with the origin and pedigree records of the genotypesto a greater extent.A total of 94.10% lines were successfully assigned to one or another group at a membership probability of ≥0.60. An analysis of molecular variance (AMOVA) revealed highly significant differences among populations and within individuals. Linkage disequilibrium for r and D' between loci ranged from 0 to 0.77 and 0 to 1, respectively. A marker trait association analysis carried out using a general linear model (GLM) and mixed linear model (MLM), identified 15 SSRs markers significantly associated with TLB resistance.These 15 markers were located on almost all chromosomes (Chr) except 7, 8, and 9. The phenotypic variation explained by these loci ranged from 6% (umc1367) to 26% (nc130, phi085). Maximum 7 associated markers were located together on Chr 2 and 5. The selected regions identified on Chr 2 and 5 corroborated the previous studies carried out in the Indian maize germplasm. Further, 11 candidate genes were identified to be associated with significant markers. The identified sources for TLB resistance and associated markers may be utilized in molecular breeding for the development of suitable genotypes.

摘要

玉米是世界上重要的谷类作物,可用于饲料、食品、饲料和工业原料。玉米叶枯病 (TLB) 是一种主要的叶部病害,可导致玉米产量损失超过 50%。考虑到这一点,本研究在 288 个不同的自交系中进行了玉米叶枯病抗性的分子多样性、群体结构和全基因组关联研究,这些自交系使用 89 个多态性简单序列重复 (SSR) 标记进行了基因型分析。在人工接种条件下,在两个热点位置对这些系进行了 TLB 疾病筛选。每个基因型的平均发病率 (PDI) 计算范围从 17%(UMI 1201)到 78%(IML 12-22),总体平均值为 40%。在一个基因座检测到的等位基因数量从两个到九个不等,共有 388 个等位基因。每个标记的多态信息含量 (PIC) 范围在 0.04 到 0.86 之间。在 89 个标记中,有 47 个标记高度多态性(PIC≥0.60)。这表明所使用的 SSR 标记非常有信息量,适合遗传多样性、群体结构和标记-性状关联研究。高度多态性标记的总观测杂合度为 0.98,表明所用的系是纯合的。基于邻接法聚类、因子分析和群体结构研究,将 288 个系聚类为 3-5 个组。分组模式在更大程度上与基因型的起源和系谱记录一致。在≥0.60 的成员概率下,共有 94.10%的系成功分配到一个或另一个组。基于分子方差分析(AMOVA)的分析表明,种群之间和个体内部存在高度显著的差异。标记间 r 和 D'的连锁不平衡范围分别为 0 到 0.77 和 0 到 1。使用一般线性模型 (GLM) 和混合线性模型 (MLM) 进行的标记-性状关联分析,确定了 15 个与 TLB 抗性显著相关的 SSR 标记。这 15 个标记位于除 7、8 和 9 之外的几乎所有染色体 (Chr) 上。这些位点解释的表型变异范围为 6%(umc1367)到 26%(nc130,phi085)。最多 7 个相关标记位于 Chr 2 和 5 上。在 Chr 2 和 5 上鉴定到的与候选标记相关的区域与在印度玉米种质资源中进行的先前研究相吻合。此外,鉴定到与显著标记相关的 11 个候选基因。鉴定到的 TLB 抗性来源和相关标记可用于分子育种,以开发合适的基因型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa2d/9030036/1e75942b661f/genes-13-00618-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa2d/9030036/144c4e7f37f0/genes-13-00618-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa2d/9030036/e9eaa87f43f2/genes-13-00618-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa2d/9030036/8fad91849eec/genes-13-00618-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa2d/9030036/1e75942b661f/genes-13-00618-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa2d/9030036/144c4e7f37f0/genes-13-00618-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa2d/9030036/e9eaa87f43f2/genes-13-00618-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa2d/9030036/8fad91849eec/genes-13-00618-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fa2d/9030036/1e75942b661f/genes-13-00618-g004.jpg

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