Discovery and Validation of a Recessively Inherited Major-Effect QTL Conferring Resistance to Maize Lethal Necrosis (MLN) Disease
Maize lethal necrosis (MLN) is a viral disease with a devastating effect on maize production. Developing and deploying improved varieties with resistance to the disease is important to effectively control MLN; however, little is known about the causal genes and molecular mechanism(s) underlying MLN...
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Frontiers Media S.A.
2021-11-01
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Online Access: | https://www.frontiersin.org/articles/10.3389/fgene.2021.767883/full |
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author | Ann Murithi Ann Murithi Michael S. Olsen Daniel B. Kwemoi Ogugo Veronica Berhanu Tadesse Ertiro Suresh L. M. Yoseph Beyene Biswanath Das Boddupalli M. Prasanna Manje Gowda |
author_facet | Ann Murithi Ann Murithi Michael S. Olsen Daniel B. Kwemoi Ogugo Veronica Berhanu Tadesse Ertiro Suresh L. M. Yoseph Beyene Biswanath Das Boddupalli M. Prasanna Manje Gowda |
author_sort | Ann Murithi |
collection | DOAJ |
description | Maize lethal necrosis (MLN) is a viral disease with a devastating effect on maize production. Developing and deploying improved varieties with resistance to the disease is important to effectively control MLN; however, little is known about the causal genes and molecular mechanism(s) underlying MLN resistance. Screening thousands of maize inbred lines revealed KS23-5 and KS23-6 as two of the most promising donors of MLN resistance alleles. KS23-5 and KS23-6 lines were earlier developed at the University of Hawaii, United States, on the basis of a source population constituted using germplasm from Kasetsart University, Thailand. Both linkage mapping and association mapping approaches were used to discover and validate genomic regions associated with MLN resistance. Selective genotyping of resistant and susceptible individuals within large F2 populations coupled with genome-wide association study identified a major-effect QTL (qMLN06_157) on chromosome 6 for MLN disease severity score and area under the disease progress curve values in all three F2 populations involving one of the KS23 lines as a parent. The major-effect QTL (qMLN06_157) is recessively inherited and explained 55%–70% of the phenotypic variation with an approximately 6 Mb confidence interval. Linkage mapping in three F3 populations and three F2 populations involving KS23-5 or KS23-6 as one of the parents confirmed the presence of this major-effect QTL on chromosome 6, demonstrating the efficacy of the KS23 allele at qMLN06.157 in varying populations. This QTL could not be identified in population that was not derived using KS23 lines. Validation of this QTL in six F2 populations with 20 SNPs closely linked with qMLN06.157 was further confirmed its consistent expression across populations and its recessive nature of inheritance. On the basis of the consistent and effective resistance afforded by the KS23 allele at qMLN06.157, the QTL can be used in both marker-assisted forward breeding and marker-assisted backcrossing schemes to improve MLN resistance of breeding populations and key lines for eastern Africa. |
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language | English |
last_indexed | 2024-12-21T08:35:30Z |
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spelling | doaj.art-83fa622d20954baa87ea2118b936c0d82022-12-21T19:10:05ZengFrontiers Media S.A.Frontiers in Genetics1664-80212021-11-011210.3389/fgene.2021.767883767883Discovery and Validation of a Recessively Inherited Major-Effect QTL Conferring Resistance to Maize Lethal Necrosis (MLN) DiseaseAnn Murithi0Ann Murithi1Michael S. Olsen2Daniel B. Kwemoi3Ogugo Veronica4Berhanu Tadesse Ertiro5Suresh L. M.6Yoseph Beyene7Biswanath Das8Boddupalli M. Prasanna9Manje Gowda10International Maize and Wheat Improvement Center (CIMMYT), Nairobi, KenyaDepartment of Plant Science and Crop Protection, University of Nairobi, Nairobi, KenyaInternational Maize and Wheat Improvement Center (CIMMYT), Nairobi, KenyaNational Crops Resources Research Institute (NaCRRI), Namulonge, UgandaInternational Maize and Wheat Improvement Center (CIMMYT), Nairobi, KenyaInternational Maize and Wheat Improvement Center (CIMMYT), Nairobi, KenyaInternational Maize and Wheat Improvement Center (CIMMYT), Nairobi, KenyaInternational Maize and Wheat Improvement Center (CIMMYT), Nairobi, KenyaInternational Maize and Wheat Improvement Center (CIMMYT), Nairobi, KenyaInternational Maize and Wheat Improvement Center (CIMMYT), Nairobi, KenyaInternational Maize and Wheat Improvement Center (CIMMYT), Nairobi, KenyaMaize lethal necrosis (MLN) is a viral disease with a devastating effect on maize production. Developing and deploying improved varieties with resistance to the disease is important to effectively control MLN; however, little is known about the causal genes and molecular mechanism(s) underlying MLN resistance. Screening thousands of maize inbred lines revealed KS23-5 and KS23-6 as two of the most promising donors of MLN resistance alleles. KS23-5 and KS23-6 lines were earlier developed at the University of Hawaii, United States, on the basis of a source population constituted using germplasm from Kasetsart University, Thailand. Both linkage mapping and association mapping approaches were used to discover and validate genomic regions associated with MLN resistance. Selective genotyping of resistant and susceptible individuals within large F2 populations coupled with genome-wide association study identified a major-effect QTL (qMLN06_157) on chromosome 6 for MLN disease severity score and area under the disease progress curve values in all three F2 populations involving one of the KS23 lines as a parent. The major-effect QTL (qMLN06_157) is recessively inherited and explained 55%–70% of the phenotypic variation with an approximately 6 Mb confidence interval. Linkage mapping in three F3 populations and three F2 populations involving KS23-5 or KS23-6 as one of the parents confirmed the presence of this major-effect QTL on chromosome 6, demonstrating the efficacy of the KS23 allele at qMLN06.157 in varying populations. This QTL could not be identified in population that was not derived using KS23 lines. Validation of this QTL in six F2 populations with 20 SNPs closely linked with qMLN06.157 was further confirmed its consistent expression across populations and its recessive nature of inheritance. On the basis of the consistent and effective resistance afforded by the KS23 allele at qMLN06.157, the QTL can be used in both marker-assisted forward breeding and marker-assisted backcrossing schemes to improve MLN resistance of breeding populations and key lines for eastern Africa.https://www.frontiersin.org/articles/10.3389/fgene.2021.767883/fullmaize lethal necrosisgenome-wide association studyF2 populationselective genotypingdisease resistance |
spellingShingle | Ann Murithi Ann Murithi Michael S. Olsen Daniel B. Kwemoi Ogugo Veronica Berhanu Tadesse Ertiro Suresh L. M. Yoseph Beyene Biswanath Das Boddupalli M. Prasanna Manje Gowda Discovery and Validation of a Recessively Inherited Major-Effect QTL Conferring Resistance to Maize Lethal Necrosis (MLN) Disease Frontiers in Genetics maize lethal necrosis genome-wide association study F2 population selective genotyping disease resistance |
title | Discovery and Validation of a Recessively Inherited Major-Effect QTL Conferring Resistance to Maize Lethal Necrosis (MLN) Disease |
title_full | Discovery and Validation of a Recessively Inherited Major-Effect QTL Conferring Resistance to Maize Lethal Necrosis (MLN) Disease |
title_fullStr | Discovery and Validation of a Recessively Inherited Major-Effect QTL Conferring Resistance to Maize Lethal Necrosis (MLN) Disease |
title_full_unstemmed | Discovery and Validation of a Recessively Inherited Major-Effect QTL Conferring Resistance to Maize Lethal Necrosis (MLN) Disease |
title_short | Discovery and Validation of a Recessively Inherited Major-Effect QTL Conferring Resistance to Maize Lethal Necrosis (MLN) Disease |
title_sort | discovery and validation of a recessively inherited major effect qtl conferring resistance to maize lethal necrosis mln disease |
topic | maize lethal necrosis genome-wide association study F2 population selective genotyping disease resistance |
url | https://www.frontiersin.org/articles/10.3389/fgene.2021.767883/full |
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