Genome assembly of Medicago truncatula accession SA27063 provides insight into spring black stem and leaf spot disease resistance.

Disease resistance Genome assembly Medicago truncatula Necrotroph Spring black stem and leaf spot disease

Journal

BMC genomics
ISSN: 1471-2164
Titre abrégé: BMC Genomics
Pays: England
ID NLM: 100965258

Informations de publication

Date de publication:
23 Feb 2024
Historique:
received: 02 01 2024
accepted: 10 02 2024
medline: 24 2 2024
pubmed: 24 2 2024
entrez: 23 2 2024
Statut: epublish

Résumé

Medicago truncatula, model legume and alfalfa relative, has served as an essential resource for advancing our understanding of legume physiology, functional genetics, and crop improvement traits. Necrotrophic fungus, Ascochyta medicaginicola, the causal agent of spring black stem (SBS) and leaf spot is a devasting foliar disease of alfalfa affecting stand survival, yield, and forage quality. Host resistance to SBS disease is poorly understood, and control methods rely on cultural practices. Resistance has been observed in M. truncatula accession SA27063 (HM078) with two recessively inherited quantitative-trait loci (QTL), rnpm1 and rnpm2, previously reported. To shed light on host resistance, we carried out a de novo genome assembly of HM078. The genome, referred to as MtHM078 v1.0, is comprised of 23 contigs totaling 481.19 Mbp. Notably, this assembly contains a substantial amount of novel centromere-related repeat sequences due to deep long-read sequencing. Genome annotation resulted in 98.4% of BUSCO fabales proteins being complete. The assembly enabled sequence-level analysis of rnpm1 and rnpm2 for gene content, synteny, and structural variation between SBS-resistant accession SA27063 (HM078) and SBS-susceptible accession A17 (HM101). Fourteen candidate genes were identified, and some have been implicated in resistance to necrotrophic fungi. Especially interesting candidates include loss-of-function events in HM078 because they fit the inverse gene-for-gene model, where resistance is recessively inherited. In rnpm1, these include a loss-of-function in a disease resistance gene due to a premature stop codon, and a 10.85 kbp retrotransposon-like insertion disrupting a ubiquitin conjugating E2. In rnpm2, we identified a frameshift mutation causing a loss-of-function in a glycosidase, as well as a missense and frameshift mutation altering an F-box family protein. This study generated a high-quality genome of HM078 and has identified promising candidates, that once validated, could be further studied in alfalfa to enhance disease resistance.

Identifiants

pubmed: 38395768
doi: 10.1186/s12864-024-10112-9
pii: 10.1186/s12864-024-10112-9
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

204

Informations de copyright

© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.

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Auteurs

Jacob R Botkin (JR)

Department of Plant Pathology, University of Minnesota, St. Paul, MN, 55108, USA.

Andrew D Farmer (AD)

National Center for Genome Resources, Santa Fe, NM, 87505, USA.

Nevin D Young (ND)

Department of Plant Pathology, University of Minnesota, St. Paul, MN, 55108, USA.

Shaun J Curtin (SJ)

United States Department of Agriculture, Plant Science Research Unit, St Paul, MN, 55108, USA. shaun.curtin@usda.gov.
Department of Agronomy and Plant Genetics, University of Minnesota, St. Paul, MN, 55108, USA. shaun.curtin@usda.gov.
Center for Plant Precision Genomics, University of Minnesota, St. Paul, MN, 55108, USA. shaun.curtin@usda.gov.
Center for Genome Engineering, University of Minnesota, St. Paul, MN, 55108, USA. shaun.curtin@usda.gov.

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