Variation in plant Toll/Interleukin-1 receptor domain protein dependence on ENHANCED DISEASE SUSCEPTIBILITY 1.
Variation in plant Toll/Interleukin-1 receptor domain protein dependence on ENHANCED DISEASE SUSCEPTIBILITY 1.
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DOI:
10.1093/plphys/kiac480
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发表时间:
2023-01-02
期刊:
影响因子:
7.4
通讯作者:
Lapin, Dmitry
中科院分区:
文献类型:
--
作者:
Johanndrees, Oliver;Baggs, Erin L.;Uhlmann, Charles;Locci, Federica;Laessle, Henriette L.;Melkonian, Katharina;Kaeufer, Kiara;Dongus, Joram A.;Nakagami, Hirofumi;Krasileva, Ksenia, V;Parker, Jane E.;Lapin, Dmitry
Toll/Interleukin-1 receptor (TIR) domains are integral to immune systems across all kingdoms. In plants, TIRs are present in nucleotide-binding leucine-rich repeat (NLR) immune receptors, NLR-like, and TIR-only proteins. Although TIR-NLR and TIR signaling in plants require the ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1) protein family, TIRs persist in species that have no EDS1 members. To assess whether particular TIR groups evolved with EDS1, we searched for TIR-EDS1 co-occurrence patterns. Using a large-scale phylogenetic analysis of TIR domains from 39 algal and land plant species, we identified 4 TIR families that are shared by several plant orders. One group occurred in TIR-NLRs of eudicots and another in TIR-NLRs across eudicots and magnoliids. Two further groups were more widespread. A conserved TIR-only group co-occurred with EDS1 and members of this group elicit EDS1-dependent cell death. In contrast, a maize (Zea mays) representative of TIR proteins with tetratricopeptide repeats was also present in species without EDS1 and induced EDS1-independent cell death. Our data provide a phylogeny-based plant TIR classification and identify TIRs that appear to have evolved with and are dependent on EDS1, while others have EDS1-independent activity. Plant Toll/Interleukin-1 receptor domain proteins can use different mechanisms to induce cell death.
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影响因子:
16.6
作者:
Bhandari, Deepak D.;Lapin, Dmitry;Parker, Jane E.
通讯作者:
Parker, Jane E.
影响因子:
4.6
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影响因子:
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通讯作者:
Milbrandt J
影响因子:
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通讯作者:
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影响因子:
82.9
作者:
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通讯作者:
Miethke, Thomas