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一 脱落酸The simple model of ABA signal in stomatal guard cells. Net effect is the lose of potassium ion and the anion (Cl -&so on)in cells. cADPR-Cyclic ADP Ribose. IP3- inositol(1,4,5)-trisphosphat.NO- nitric oxide. PA- Acide Phosphatidique. PLC- Phospholipase C. PLD- Phospholipase D. R- receptor. ROS- reactive oxygen species. S1P- Sphingosine 1-phosphate. Biding of ABA and receptor(in order to see better, only show the extracellular receptor); After ABA combining receptor, the ROS is induced to produce. Then the Ca+ channels is activated on the plasma membrane, ROS is produced by PID which mediated phosphatidic acid; The Ca+ internal flow caused instantaneous changes of intracellular calcium. That promoted the release of calcium from vacuoles. ABA is to stimulate the product of NO, and NO add cADPR. ABA add IP3 by including S1p, the heterogeneous co-polymer and PLD,PLC. The rise of cADPR and IP3 activate other calcium channel of the vacuole membrane, more CA+ release from vacuoles.The rise of intracellular calcium blocking the channels of K+ on the plasma membrane.The rise of intracellular calcium to promote open Cl- channels on the plasma membraneProton pump on the plasma membrane is restrained by ABA induced of intracellular calcium increase and inhibition of intracellular pH increased, plasma membrane depolarization further.K+ and anion from across the plasma membrane vacuole first released into the cytoplasm.二 生长素Auxin and TIR1/ABF receptor activation after auxin response model of gene transcription。1. In the absence of auxin, AUX /IAA deter that the ARF transcription activation combined with the formation of inactive form to suppress the auxin induction of gene transcription. Auxin and SCFTIR1 united that promote them interaction with AUX/IAA.2. Auxin activated SCFTIR1 complex whole made the ubiquitin molecules linked to AUX/IAA. Promoting AUX/IAA degrade by protease. AUX/IAA maked the ARF transcriptional activation protein removal and degradation.3. In most of the induced by auxin genes, two ARF protein molecules activined dimer, to further promoted gene transcription.三 赤霉素1.GAI combined with aleurone cells on the surface of the membrane receptor2. GA receptors on the surface made protein interactions with the cell complex and heterogeneous trimer G. 3. What rely on calcium signal transduction pathways is consisted of cGMP and some other components, they interact with SCF ubiquitin is connect F -box protein.4. GAI could also directly into the cell and unite a main position receptor proteins on nuclear. 5. Active F-box protein and a DELLA domain protein suppressor proteins are united, bocked the GAMYB gene transcription. DELLA domain proteins repressor may block the activity of a transcription of catalyst.6. Inhibitory factor is degradated by SCF ubiquitin ligase compounds7. The degradation of repressor made GAMYB and other responsed gene expressed.8.The new GAMYB protein get in the nucleus ,united -amylase-promoter and other responsed gene. 9. Gene transcription is activated10. -Amylase and other dehydrogenase gene are synthesized in the rough endoplasmic reticulum. 11. Proteins secreted by the golgi apparatus. 12. The secretion pathway need GA activated which depends on the way of calmodulin kinase of participation.四 油菜素甾醇BR is sterol (Brassinosteroids, BRs) is a kind of important plant sterols hormone, mainly adjust the plant height, plant type, sterility, flowering time, plant growth and development of many aspects, such as the ageing process and regulation of plant adaptability to the environment.BR signal which is located in the cell membrane receptor kinase BRI1, previous research has found that BKI1 (BRI1 kinase inhibitor 1) is the key of BRI1 negative regulatory proteins, in the absence of BR, and BKI1 positioning on the membrane receptor BRI1 interactions, thus inhibiting the activity of BRI1 and BR signal transduction;When there is BR signal, BKI1 into the cytoplasm from the cell membrane dissociation and lift its inhibition of BRI1, thus BR signaling pathway is activated.When no BR, BKI1 and 14-3-3 protein inhibiting BR receptor BRI1 and transcription factors respectively BES1;Promote the phosphorylation of BKI1, BR signal phosphorylation of BKI1 with the 14-3-3 dissociation in the cytoplasm, so as to lift its inhibition of BRI1 and BES1, promote BR signal output).五 细胞分裂素1 Cytokinins combined into CRE1 dimers, CRE1 extracellular parts called CHASE area, the other two receptor kinase(AHKZ , AHK3 ) may serve as Arabidopsis Cytokinin receptor.2 The combination of cytokinin and the receptor activate histidine kinase activity, phosphate group was transferred to the domain on the Aspartic Acid.3 Phosphate group was transferred to the AHP protein conservative histidine.4 Protein phosphorylation lead AHP into the nucleus, the phosphate groups transferred to the type B ARR accept domain Aspartic Acid. 5 The type B ARR phosphorylation activated the output field, induced thetype A ARRs gene transcription.6 The type A ARR was phosphorylated by AHP protein. 7 Phosphorylation of type A ARR interact with other factors mediated cytokinins caused by changes in cell function.六 乙烯Ethylene receptor (ETR1, ERS, ETR2, EIN4 and ERS2) is located in the endoplasmic reticulum omentum, its structure and similar to histidine kinases in bacterial two-component signaling system.In the absence of ethylene, ethylene receptor itself is in a state of activation, the function of the class can activate the Raf kinase CTR1.CTR1 is inhibiting factor in ethylene signaling pathways, it can be located on the endoplasmic reticulum retinal phosphorylation also EIN2 the c-terminal domain structure (C - terminal end of EIN2, CEND).EIN2 is a key component of ethylene signal transduction, its CEND is thought to participate in the ethylene signal transduction, ectopic expression can CEND part ethylene reaction activation.Be CTR1 CEND can be F - box after the phosphorylated proteins EIN2 TARGETING PROTEIN1 (ETP1/2) / 2 to identify and enter the proteasome degradation.Therefore, in the absence of vinyl, CTR1 by inhibiting EIN2 the ethylene signaling pathway in the closed state.When there is ethylene, ethylene and the receptor and the receptors and CTR1 inactivation, CTR1 phosphorylation of EIN2 suppressed.EIN2 CEND through shear off from endoplasm retinal, part CEND with EBF1/2 mRNA 3 UTRs combination with EIN5 P - such as body protein interactions, enter the P - body, thus inhibiting EBF1/2 mRNA translation, and cut off the EBF pro
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