<?xml version="1.0" encoding="UTF-8"?><rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcq="http://purl.org/dc/terms/"><records count="1" morepages="false" start="1" end="1"><record rownumber="1"><dc:product_type>Journal Article</dc:product_type><dc:title>Plant “helper” immune receptors are Ca &lt;sup&gt;2+&lt;/sup&gt; -permeable nonselective cation channels</dc:title><dc:creator>Jacob, Pierre; Kim, Nak Hyun; Wu, Feihua; El-Kasmi, Farid; Chi, Yuan; Walton, William G.; Furzer, Oliver J.; Lietzan, Adam D.; Sunil, Sruthi; Kempthorn, Korina; Redinbo, Matthew R.; Pei, Zhen-Ming; Wan, Li; Dangl, Jeffery L.</dc:creator><dc:corporate_author/><dc:editor/><dc:description>Plant nucleotide-binding leucine-rich repeat receptors (NLRs) regulate immunity and cell death. In              Arabidopsis              , a subfamily of “helper” NLRs is required by many “sensor” NLRs. Active NRG1.1 oligomerized, was enriched in plasma membrane puncta, and conferred cytoplasmic calcium ion (Ca              2+              ) influx in plant and human cells. NRG1.1-dependent Ca              2+              influx and cell death were sensitive to Ca              2+              channel blockers and were suppressed by mutations affecting oligomerization or plasma membrane enrichment. Ca              2+              influx and cell death mediated by NRG1.1 and ACTIVATED DISEASE RESISTANCE 1 (ADR1), another helper NLR, required conserved negatively charged N-terminal residues. Whole-cell voltage-clamp recordings demonstrated that              Arabidopsis              helper NLRs form Ca              2+              -permeable cation channels to directly regulate cytoplasmic Ca              2+              levels and consequent cell death. Thus, helper NLRs transduce cell death signals directly.</dc:description><dc:publisher/><dc:date>2021-07-23</dc:date><dc:nsf_par_id>10323914</dc:nsf_par_id><dc:journal_name>Science</dc:journal_name><dc:journal_volume>373</dc:journal_volume><dc:journal_issue>6553</dc:journal_issue><dc:page_range_or_elocation>420 to 425</dc:page_range_or_elocation><dc:issn>0036-8075</dc:issn><dc:isbn/><dc:doi>https://doi.org/10.1126/science.abg7917</dc:doi><dcq:identifierAwardId>1758400</dcq:identifierAwardId><dc:subject/><dc:version_number/><dc:location/><dc:rights/><dc:institution/><dc:sponsoring_org>National Science Foundation</dc:sponsoring_org></record></records></rdf:RDF>