A key event that follows pathogen recognition by a resistance(R)protein containing an NB-ARC(nucleotide-binding adaptor shared by Apaf-1,R proteins,and Ced-4)domain is hypersensitive response(HR)-type cell death accom...A key event that follows pathogen recognition by a resistance(R)protein containing an NB-ARC(nucleotide-binding adaptor shared by Apaf-1,R proteins,and Ced-4)domain is hypersensitive response(HR)-type cell death accompanied by accumulation of reactive oxygen species and nitric oxide.However,the integral mechanisms that underlie this process remain relatively opaque.Here,we show that a gain-offunction mutation in the NB-ARC protein RLS1(Rapid Leaf Senescence 1)triggers high-light-dependent HR-like cell death in rice.The RLS1-mediated defense response is largely independent of salicylic acid accumulation,NPR1(Nonexpressor of Pathogenesis-Related Gene 1)activity,and RAR1(Required for Mla12 Resistance 1)function.A screen for suppressors of RLS1 activation identified RMC(Root Meander Curling)as essential for the RLS1-activated defense response.RMC encodes a cysteine-rich receptor-like secreted protein(CRRSP)and functions as an RLS1-binding partner.Intriguingly,their co-expression resulted in a change in the pattern of subcellular localization and was sufficient to trigger cell death accompanied by a decrease in the activity of the antioxidant enzyme APX1.Collectively,our findings reveal an NBARC-CRRSP signaling module that modulates oxidative state,the cell death process,and associated immunity responses in rice.展开更多
基金supported by grants from the National Natural Science Foundation of China(grant numbers 31571248,31430063,and 31871586).
文摘A key event that follows pathogen recognition by a resistance(R)protein containing an NB-ARC(nucleotide-binding adaptor shared by Apaf-1,R proteins,and Ced-4)domain is hypersensitive response(HR)-type cell death accompanied by accumulation of reactive oxygen species and nitric oxide.However,the integral mechanisms that underlie this process remain relatively opaque.Here,we show that a gain-offunction mutation in the NB-ARC protein RLS1(Rapid Leaf Senescence 1)triggers high-light-dependent HR-like cell death in rice.The RLS1-mediated defense response is largely independent of salicylic acid accumulation,NPR1(Nonexpressor of Pathogenesis-Related Gene 1)activity,and RAR1(Required for Mla12 Resistance 1)function.A screen for suppressors of RLS1 activation identified RMC(Root Meander Curling)as essential for the RLS1-activated defense response.RMC encodes a cysteine-rich receptor-like secreted protein(CRRSP)and functions as an RLS1-binding partner.Intriguingly,their co-expression resulted in a change in the pattern of subcellular localization and was sufficient to trigger cell death accompanied by a decrease in the activity of the antioxidant enzyme APX1.Collectively,our findings reveal an NBARC-CRRSP signaling module that modulates oxidative state,the cell death process,and associated immunity responses in rice.
文摘黑山头组玄武岩-玄武安山岩组合是西准噶尔早石炭世海相火山-沉积建造的重要组成部分,其与高Mg安山岩及O型adakite共生。此次分析的所有样品均为玄武质岩石,Si O2含量为49.62%~55.68%,平均为52.70%;明显高Ti O2（1.16%~1.99%）,平均为1.56%;显著富Na2O而贫K2O,Na2O为3.17%~6.35%,平均为4.90%,Na2O/K2O为1.19~26.08,绝大多数样品该比值〉4（平均8.93）。样品明显富集Nb、Sr、Zr等,Nb含量均〉7×10-6（7.29×10-6~12.32×10-6,平均为9.48×10-6）;全部样品Sr均〉400×10-6（618×10-6~1107×10-6,平均为825×10-6）;Zr〉158×10-6（159×10-6~217×10-6,平均为182.6×10-6）;Zr/Y比值〉4（6.63~11.09,平均为8.62）。显著高于一般岛弧玄武质岩类。轻稀土明显富集而重稀土亏损显著,且有基本一致的弱正Eu异常。（La/Nb）PM比值〉0.7（1.23~2.26,平均1.94）,（87Sr/86Sr）i=0.7035~0.7039;143Nd/144Nd=0.5128~0.5129;εNd（t）=5.49~7.13。这些地球化学特征与Sajona et al.（1993,1994,1996）确立的富Nb岛弧玄武岩基本一致,而与一般岛弧玄武岩有显著区别。这一发现,为确认西准噶尔早石炭世存在富Nb岛弧玄武岩提供了地球化学佐证,丰富了新疆乃至我国富Nb岛弧玄武岩的产地与层位,也为确认本区早石炭世岛弧构造环境提供了重要依据。
