Mutations in DNA polymerase δ subunit 1 co-segregate with CMD2-type resistance to Cassava Mosaic Geminiviruses

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作者
Yi-Wen Lim
Ben N. Mansfeld
Pascal Schläpfer
Kerrigan B. Gilbert
Narayanan N. Narayanan
Weihong Qi
Qi Wang
Zhenhui Zhong
Adam Boyher
Jackson Gehan
Getu Beyene
Zuh-Jyh Daniel Lin
Williams Esuma
Suhua Feng
Christelle Chanez
Nadine Eggenberger
Gerald Adiga
Titus Alicai
Steven E. Jacobsen
Nigel J. Taylor
Wilhelm Gruissem
Rebecca S. Bart
机构
[1] ETH Zürich,Institute of Molecular Plant Biology, Department of Biology
[2] Donald Danforth Plant Science Center,Functional Genomics Center Zurich
[3] ETH Zurich and University of Zurich,Department of Molecular, Cell and Developmental Biology
[4] University of California Los Angeles,Root Crops Program
[5] National Crops Resources Research Institute,Biotechnology Center
[6] Howard Hughes Medical Institute University of California Los Angeles,undefined
[7] National Chung Hsing University,undefined
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摘要
Cassava mosaic disease (CMD) suppresses cassava yields across the tropics. The dominant CMD2 locus confers resistance to cassava mosaic geminiviruses. It has been reported that CMD2-type landraces lose resistance after regeneration through de novo morphogenesis. As full genome bisulfite sequencing failed to uncover an epigenetic mechanism for this loss of resistance, whole genome sequencing and genetic variant analysis was performed and the CMD2 locus was fine-mapped to a 190 kilobase interval. Collectively, these data indicate that CMD2-type resistance is caused by a nonsynonymous, single nucleotide polymorphism in DNA polymerase δ subunit 1 (MePOLD1) located within this region. Virus-induced gene silencing of MePOLD1 in a CMD-susceptible cassava variety produced a recovery phenotype typical of CMD2-type resistance. Analysis of other CMD2-type cassava varieties identified additional candidate resistance alleles within MePOLD1. Genetic variation of MePOLD1, therefore, could represent an important genetic resource for resistance breeding and/or genome editing, and elucidating mechanisms of resistance to geminiviruses.
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