PIF4 Dotaz Zobrazit nápovědu
Brassinosteroids (BRs) are essential phytohormones regulating various developmental and physiological processes during normal growth and development.cog1-3D(cogwheel1-3D) was identified as an activation-tagged genetic modifier ofbri1-5, an intermediate BR receptor mutant in Arabidopsis (Arabidopsis thaliana).COG1encodes a Dof-type transcription factor found previously to act as a negative regulator of the phytochrome signaling pathway.cog1-3Dsingle mutants show an elongated hypocotyl phenotype under light conditions. A loss-of-function mutant or inducible expression of a dominant negative form ofCOG1in the wild type results in an opposite phenotype. A BR profile assay indicated that BR levels are elevated incog1-3Dseedlings. Quantitative reverse transcription-polymerase chain reaction analyses showed that several key BR biosynthetic genes are significantly up-regulated incog1-3Dcompared with those of the wild type. Two basic helix-loop-helix transcription factors,PIF4andPIF5, were found to be transcriptionally up-regulated incog1-3DGenetic analysis indicated that PIF4 and PIF5 were required for COG1 to promote BR biosynthesis and hypocotyl elongation. Chromatin immunoprecipitation and electrophoretic mobility shift assays indicated that COG1 binds to the promoter regions ofPIF4andPIF5, and PIF4 and PIF5 bind to the promoter regions of key BR biosynthetic genes, such asDWF4andBR6ox2, to directly promote their expression. These results demonstrated that COG1 regulates BR biosynthesis via up-regulating the transcription ofPIF4andPIF5.
- MeSH
- Arabidopsis genetika metabolismus MeSH
- biologické modely MeSH
- biosyntetické dráhy genetika MeSH
- bodová mutace genetika MeSH
- brassinosteroidy biosyntéza MeSH
- ethylmethansulfonát MeSH
- fenotyp MeSH
- hypokotyl růst a vývoj metabolismus MeSH
- promotorové oblasti (genetika) genetika MeSH
- proteiny huseníčku genetika metabolismus MeSH
- regulace genové exprese u rostlin MeSH
- rostlinné geny MeSH
- sekvence nukleotidů MeSH
- suprese genetická MeSH
- transkripční faktory bHLH genetika metabolismus MeSH
- transkripční faktory genetika metabolismus MeSH
- upregulace genetika MeSH
- vazba proteinů genetika MeSH
- Publikační typ
- časopisecké články MeSH
Auxin is necessary for the inhibition of root growth induced by aluminium (Al) stress, however the molecular mechanism controlling this is largely unknown. Here, we report that YUCCA (YUC), which encodes flavin monooxygenase-like proteins, regulates local auxin biosynthesis in the root apex transition zone (TZ) in response to Al stress. Al stress up-regulates YUC3/5/7/8/9 in the root-apex TZ, which we show results in the accumulation of auxin in the root-apex TZ and root-growth inhibition during the Al stress response. These Al-dependent changes in the regulation of YUCs in the root-apex TZ and YUC-regulated root growth inhibition are dependent on ethylene signalling. Increasing or disruption of ethylene signalling caused either enhanced or reduced up-regulation, respectively, of YUCs in root-apex TZ in response to Al stress. In addition, ethylene enhanced root growth inhibition under Al stress was strongly alleviated in yuc mutants or by co-treatment with yucasin, an inhibitor of YUC activity, suggesting a downstream role of YUCs in this process. Moreover, ethylene-insensitive 3 (EIN3) is involved into the direct regulation of YUC9 transcription in this process. Furthermore, we demonstrated that PHYTOCHROME INTERACTING FACTOR4 (PIF4) functions as a transcriptional activator for YUC5/8/9. PIF4 promotes Al-inhibited primary root growth by regulating the local expression of YUCs and auxin signal in the root-apex TZ. The Al-induced expression of PIF4 in root TZ acts downstream of ethylene signalling. Taken together, our results highlight a regulatory cascade for YUCs-regulated local auxin biosynthesis in the root-apex TZ mediating root growth inhibition in response to Al stress.
- MeSH
- aktivace transkripce genetika MeSH
- Arabidopsis účinky léků genetika růst a vývoj MeSH
- ethyleny metabolismus MeSH
- fyziologický stres genetika MeSH
- hliník toxicita MeSH
- jaderné proteiny genetika metabolismus MeSH
- kořeny rostlin účinky léků genetika růst a vývoj MeSH
- kyseliny indoloctové metabolismus MeSH
- oxygenasy genetika MeSH
- proteiny huseníčku genetika metabolismus MeSH
- regulace genové exprese u rostlin účinky léků MeSH
- signální transdukce genetika MeSH
- transkripční faktory bHLH genetika metabolismus MeSH
- transkripční faktory genetika metabolismus MeSH
- Publikační typ
- časopisecké články MeSH
The plant-specific receptor-like cytoplasmic kinases (RLCKs) form a large, poorly characterized family. Members of the RLCK VI_A class of dicots have a unique characteristic: their activity is regulated by Rho-of-plants (ROP) GTPases. The biological function of one of these kinases was investigated using a T-DNA insertion mutant and RNA interference. Loss of RLCK VI_A2 function resulted in restricted cell expansion and seedling growth. Although these phenotypes could be rescued by exogenous gibberellin, the mutant did not exhibit lower levels of active gibberellins nor decreased gibberellin sensitivity. Transcriptome analysis confirmed that gibberellin is not the direct target of the kinase; its absence rather affected the metabolism and signalling of other hormones such as auxin. It is hypothesized that gibberellins and the RLCK VI_A2 kinase act in parallel to regulate cell expansion and plant growth. Gene expression studies also indicated that the kinase might have an overlapping role with the transcription factor circuit (PIF4-BZR1-ARF6) controlling skotomorphogenesis-related hypocotyl/cotyledon elongation. Furthermore, the transcriptomic changes revealed that the loss of RLCK VI_A2 function alters cellular processes that are associated with cell membranes, take place at the cell periphery or in the apoplast, and are related to cellular transport and/or cell wall reorganisation.
- MeSH
- Arabidopsis účinky léků enzymologie genetika růst a vývoj MeSH
- DNA bakterií genetika metabolismus MeSH
- DNA vazebné proteiny genetika metabolismus MeSH
- geneticky modifikované rostliny MeSH
- gibereliny metabolismus farmakologie MeSH
- hypokotyl účinky léků enzymologie genetika růst a vývoj MeSH
- inzerční mutageneze MeSH
- kotyledon účinky léků enzymologie genetika růst a vývoj MeSH
- kyseliny indoloctové metabolismus farmakologie MeSH
- protein-serin-threoninkinasy genetika metabolismus MeSH
- proteiny huseníčku genetika metabolismus MeSH
- regulace genové exprese u rostlin * MeSH
- regulátory růstu rostlin farmakologie MeSH
- semenáček účinky léků enzymologie genetika růst a vývoj MeSH
- stanovení celkové genové exprese MeSH
- transkripční faktory bHLH genetika metabolismus MeSH
- transkripční faktory genetika metabolismus MeSH
- transkriptom MeSH
- vývojová regulace genové exprese MeSH
- Publikační typ
- časopisecké články MeSH