Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.13.3 (histidine kinase)
 2,405 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fusarium graminearum produces trichothecenes in aerial hyphae, a process which is markedly suppressed by NaCl without a significant effect on fungal growth. Here we report on the involvement of kinases of the two-component osmotic signal transduction pathway in the regulation of secondary metabolism in F. graminearum. While a deletion null mutant of FgOs1 (encoding the osmosensor histidine kinase) (deltaFgOs1) produced a reduced amount of the red pigment aurofusarin and was unaltered in its ability to produce trichothecenes, deletion null mutants of FgOs4 (encoding mitogen-activated protein kinase kinase kinase; MAPKKK), FgOs5 (MAPKK), and FgOs2 (MAPK) showed markedly enhanced pigmentation and failed to produce trichothecenes in aerial hyphae. Also, the transcript levels of PKS12 and GIP2 (aurofusarin biosynthetic pathway and regulatory genes, respectively) were significantly enhanced in the deltaFgOs4, deltaFgOs5, and deltaFgOs2 mutants and were reduced in the deltaFgOs1 mutant. In addition, expression of Tri4 and Tri6 (trichothecene biosynthetic pathway and regulatory genes) and production of trichothecenes in rice medium were markedly reduced in the former three protein kinase mutants. This is the first report demonstrating the involvement of a MAPK in the regulation of secondary metabolism.
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PMID:Involvement of the osmosensor histidine kinase and osmotic stress-activated protein kinases in the regulation of secondary metabolism in Fusarium graminearum. 1789 20

The mitogen-activated protein kinase kinase kinase (MAPKKK) Constitutive Triple-Response1 (CTR1) plays a key role in mediating ethylene receptor signaling via its N-terminal interaction with the ethylene receptor C-terminal histidine kinase (HK) domain. Loss-of-function mutations of CTR1 prevent ethylene receptor signaling, and corresponding ctr1 mutants show a constitutive ethylene response phenotype. We recently reported in Plant Physiology that expression of the truncated ethylene receptor Ethylene Response1 (ETR1) isoforms etr1 ( 1-349) and dominant ethylene-insensitive etr1-1 ( 1-349) , lacking the C-terminal HK and receiver domains, both suppressed the ctr1 mutant phenotype. Therefore, the ETR1 N terminus is capable of receptor signaling independent of CTR1. The constitutive ethylene response phenotype is stronger for ctr1-1 than ctr1-1 lines expressing the etr1 ( 1-349) transgene, so N-terminal signaling by the full-length but not truncated ETR1 is inhibited by ctr1-1. We address possible modulations of ETR1 N-terminal signaling with docking of CTR1 on the ETR1 HK domain.
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PMID:Possible modulation of Arabidopsis ETR1 N-terminal signaling by CTR1. 2290 95