Dysfunction of Arabidopsis MACPF domain protein activates programmed cell death via tryptophan metabolism in MAMP-triggered immunity
PBN-AR
Instytucja
Instytut Chemii Bioorganicznej Polskiej Akademii Nauk
Informacje podstawowe
Główny język publikacji
en
Czasopismo
PLANT JOURNAL (45pkt w roku publikacji)
ISSN
0960-7412
EISSN
1365-313X
Wydawca
WILEY-BLACKWELL
DOI
URL
Rok publikacji
2017
Numer zeszytu
2
Strony od-do
381-393
Numer tomu
89
Identyfikator DOI
Liczba arkuszy
Słowa kluczowe
angielski
cell death
Colletotrichum orbiculare
MACPF domain
MAMPs
salicylic acid signaling
secondary metabolites
Tryptophan-derived metabolism
Streszczenia
Język
en
Treść
Plant immune responses triggered upon recognition of microbe-associated molecular patterns (MAMPs) typically restrict pathogen growth without a host cell death response. We isolated two Arabidopsis mutants, derived from accession Col-0, that activated cell death upon inoculation with nonadapted fungal pathogens. Notably, the mutants triggered cell death also when treated with bacterial MAMPs such as flg22. Positional cloning identified NSL1 (Necrotic Spotted Lesion 1) as a responsible gene for the phenotype of the two mutants, whereas nsl1 mutations of the accession No-0 resulted in necrotic lesion formation without pathogen inoculation. NSL1 encodes a protein of unknown function containing a putative membrane-attack complex/perforin (MACPF) domain. The application of flg22 increased salicylic acid (SA) accumulation in the nsl1 plants derived from Col-0, while depletion of isochorismate synthase 1 repressed flg22-inducible lesion formation, indicating that elevated SA is needed for the cell death response. nsl1 plants of Col-0 responded to flg22 treatment with an RBOHD-dependent oxidative burst, but this response was dispensable for the nsl1-dependent cell death. Surprisingly, loss-of-function mutations in PEN2, involved in the metabolism of tryptophan (Trp)-derived indole glucosinolates, suppressed the flg22-induced and nsl1-dependent cell death. Moreover, the increased accumulation of SA in the nsl1 plants was abrogated by blocking Trp-derived secondary metabolite biosynthesis, whereas the nsl1-dependent hyperaccumulation of PEN2-dependent compounds was unaffected when the SA biosynthesis pathway was blocked. Collectively, these findings suggest that MAMP-triggered immunity activates a genetically programmed cell death in the absence of the functional MACPF domain protein NSL1 via Trp-derived secondary metabolite-mediated activation of the SA pathway.
Inne
System-identifier
PX-58c2885dd5dead78c0210a99
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