Skip to main content
ARS Home » Plains Area » Fargo, North Dakota » Edward T. Schafer Agricultural Research Center » Cereal Crops Improvement Research » Research » Publications at this Location » Publication #415388
Research Project: Improvement of Disease and Pest Resistance in Barley, Durum, Oat, and Wheat Using Genetics and Genomics

Location: Cereal Crops Improvement Research

Title: Map-based cloning of the Nec50 gene which regulates programmed cell death in barley

Author
item D'EUSTACHIO, ABBY - North Dakota State University
item LIU, ZHAOHUI - North Dakota State University
item Yang, Shengming

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 6/1/2024
Publication Date: 6/10/2024
Citation: D'Eustachio, A., Liu, Z., Yang, S. 2024. Map-based cloning of the Nec50 gene which regulates programmed cell death in barley. Meeting Abstract. 2024 Annual Meeting of the North Central Division of the American Phytopathological Society.

Interpretive Summary:

Technical Abstract: In plants, the hypersensitive response (HR) is associated a rapid programmed cell death (PCD) in response to pathogen attack. Biotrophic pathogens require living host cells, and the elicited PCD deprives nutrients from them, thus suppressing their colonization process. In contrast, necrotrophic pathogens kill host cells and feed on dead tissues thus PCD benefits them.. Understanding of the PCD mechanism is important to manipulate resistance and susceptibility pathways for the purpose of disease control. However, PCD signaling remains largely unknown. Lesion mimic mutants (LMM), exhibiting necrotic lesions spontaneously without pathogen infection, provide a powerful tool to identify genes or cellular events that regulate cell death in plant. In the present study, we cloned the Nec50 gene which is a negative suppressor of PCD in barley. Loss-of-function mutation in Nec50 caused by EMS mutagenesis results in the formation of tan to light brown lesions on the leaf at the jointing stage, which enlarge rapidly and coalesce after heading, leading to premature leaf senesce. Genetic mapping delimited Nec50 to a 3M-bp region on chromosome 7H. RNA-seq analysis and mutseq technique allow us to identify a single point mutation of C'T transition at the 5’UTR of HORVU.MOREX.r3.7HG0668180, which encodes a putative O-fucosyltransferase 15-like protein. CRISPR-mediated gene mutagenesis of this gene phenocopied the nec50 mutant, validating that HORVU.MOREX.r3.7HG0668180 is the Nec50 gene indeed. Therefore, cloning of Nec50 in the present study highlights an important role of cellular fucosylation in regulating programmed cell death, shedding light on molecular mechanisms of plant defenses.