NAD + cleavage activity by animal and plant TIR domains in cell death pathways
Author(s) -
S. Horsefield,
Hayden Burdett,
Xiaoxiao Zhang,
M.K. Manik,
Yun Shi,
Jian Chen,
Tiancong Qi,
Jonathan Gilley,
JhihSiang Lai,
Maxwell X. Rank,
Lachlan W. Casey,
Weixi Gu,
Daniel J. Ericsson,
Gabriel Foley,
Robert Hughes,
Todd Bosanac,
Mark von Itzstein,
John P. Rathjen,
Jeffrey D. Nanson,
Mikael Bodén,
Ian B. Dry,
Simon J. Williams,
Brian J. Staskawicz,
Michael P. Coleman,
Thomas Ve,
Peter N. Dodds,
Boštjan Kobe
Publication year - 2019
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.aax1911
Subject(s) - nad+ kinase , cofactor , nicotinamide adenine dinucleotide , biology , receptor , pathogen , programmed cell death , signal transduction , microbiology and biotechnology , biochemistry , chemistry , apoptosis , enzyme , genetics
NAD depletion as pathogen response One way that plants respond to pathogen infection is by sacrificing the infected cells. The nucleotide-binding leucine-rich repeat immune receptors responsible for this hypersensitive response carry Toll/interleukin-1 receptor (TIR) domains. In two papers, Horsefieldet al. and Wanet al. report that these TIR domains cleave the metabolic cofactor nicotinamide adenine dinucleotide (NAD+ ) as part of their cell-death signaling in response to pathogens. Similar signaling links mammalian TIR-containing proteins to NAD+ depletion during Wallerian degeneration of neurons.Science , this issue p.793 , p.799
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