Over the last few years, it has become evident that reactive oxygen species (ROS) signalling plays an important role in various physiological responses, including pathogen defense and stomatal opening/closure. On th...
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Over the last few years, it has become evident that reactive oxygen species (ROS) signalling plays an important role in various physiological responses, including pathogen defense and stomatal opening/closure. On the other hand, ROS overproduction is detrimental for proper plant growth and development, indicating that the regulation of an appropriate redox balance is essential for plants. ROS homeostasis in plants involves the mitogen-activated protein kinase (MAPK) pathway consisting of the MAPK kinase kinase MEKK1 and the MAPK MPK4. Phenotypic and molecular analysis revealed that the MAPK kinases MKK1 and MKK2 are part of a cascade, regulating ROS and salicylic acid (SA) accumulation. Gene expression analysis shows that of 32 transcription factors reported to be highly responsive to multiple ROS-inducing conditions, 20 are regulated by the MEKK1, predominantly via the MEKK1-MKK1/2-MPK4 pathway. However, MEKK1 also functions on other as yet unknown pathways and part of the MEKK1-dependent MPK4 responses are regulated independently of MKK1 and MKK2. Overall, this analysis emphasizes the central role of this MAPK cascade in oxidative stress signalling, but also indicates the high level of complexity revealed by this signalling network.
Mitogen-activated protein kinase (MAPK) cascades are universal signal transduction modules present in all eukaryotes. In plants, MAPK cascades were shown to regulate cell division, developmental processes, stress re...
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Mitogen-activated protein kinase (MAPK) cascades are universal signal transduction modules present in all eukaryotes. In plants, MAPK cascades were shown to regulate cell division, developmental processes, stress responses, and hormone pathways. The subgroup A of Arabidopsis MAPKs consists of AtMPK3, AtMPK6, and AtMPK10. AtMPK3 and AtMPK6 are activated by their upstream MAP kinase kinases (MKKs) AtMKK4 and AtMKK5 in response to biotic and abiotic stress. In addition, they were identified as key regulators of stomatal development and patterning. AtMPKIO has long been considered as a pseudo-gene, derived from a gene duplication of AtMPK6. Here we show that AtMPKIO is expressed highly but very transiently in seedlings and at sites of local auxin maxima leaves. MPK10 encodes a functional kinase and interacts with the upstream MAP kinase kinase (MAPKK) AtMKK2. mpklO mutants are delayed in flowering in long-day conditions and in continuous light. Moreover, cotyledons of mpk10 and mkk2 mutants have reduced vein complexity, which can be reversed by inhibiting polar auxin transport (PAT). Auxin does not affect AtMPKIO expression while treatment with the PAT inhibitor HFCA extends the expression in leaves and reverses the mpklO mutant phenotype. These results suggest that the AtMKK2-AtMPK10 MAPK module regulates venation complexity by altering PAT efficiency.
In plants,the antagonism between growth and defense is hardwired by hormonal *** perception of pathogen-associatedmolecularpatterns(PAMPs)frominvadingmicroorganismsinhibits auxin signalingand plant ***,pathogens manip...
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In plants,the antagonism between growth and defense is hardwired by hormonal *** perception of pathogen-associatedmolecularpatterns(PAMPs)frominvadingmicroorganismsinhibits auxin signalingand plant ***,pathogens manipulate auxin signaling to promote disease,but how this hormone inhibits immunity is not fully *** maydis is a maize pathogen that induces auxin signaling in its *** characterized a *** effector protein,Naked1(Nkd1),that is translocated into the host *** its native ethylene-responsive element binding factor-associated amphiphilic repression(EAR)motif,Nkd1 binds to the transcriptional co-repressors TOPLESS/TOPLESS-related(TPL/TPRs)and prevents the recruitment of a transcriptional repressor involved in hormonal signaling,leading to the derepression of auxin and jasmonate signaling and thereby promoting susceptibility to(hemi)biotrophic pathogens.A moderate upregulation of auxin signaling inhibits the PAMP-triggered reactive oxygen species(ROS)burst,an early defense ***,our findings establish a clear mechanism for auxin-induced pathogen *** Nkd1 variants with increased expression or increased EAR-mediated TPL/TPR binding trigger typical salicylic-acid-mediated defense reactions,leading to pathogen *** implies that moderate binding of Nkd1 to TPL is a result of a balancing evolutionary selection process to enable TPL manipulation while avoiding host recognition.
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