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MAP 激酶磷酸酶 1 控制气孔发育过程中的细胞命运转变。

MAP KINASE PHOSPHATASE1 Controls Cell Fate Transition during Stomatal Development.

机构信息

Department of Biology, Concordia University, Montreal, Quebec H4B 1R6, Canada.

Department of Biology, Concordia University, Montreal, Quebec H4B 1R6, Canada

出版信息

Plant Physiol. 2018 Sep;178(1):247-257. doi: 10.1104/pp.18.00475. Epub 2018 Jul 12.

DOI:10.1104/pp.18.00475
PMID:30002258
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6130035/
Abstract

Stomata on the plant epidermis control gas and water exchange and are formed by MAPK-dependent processes. Although the contribution of MAP KINASE3 (MPK3) and MPK6 (MPK3/MPK6) to the control of stomatal patterning and differentiation in Arabidopsis () has been examined extensively, how they are inactivated and regulate distinct stages of stomatal development is unknown. Here, we identify a dual-specificity phosphatase, MAP KINASE PHOSPHATASE1 (MKP1), which promotes stomatal cell fate transition by controlling MAPK activation at the early stage of stomatal development. Loss of function of creates clusters of small cells that fail to differentiate into stomata, resulting in the formation of patches of pavement cells. We show that MKP1 acts downstream of YODA (a MAPK kinase kinase) but upstream of MPK3/MPK6 in the stomatal signaling pathway and that MKP1 deficiency causes stomatal signal-induced MAPK hyperactivation in vivo. By expressing MKP1 in the three discrete cell types of stomatal lineage, we further identified that MKP1-mediated deactivation of MAPKs in early stomatal precursor cells directs cell fate transition leading to stomatal differentiation. Together, our data reveal the important role of MKP1 in controlling MAPK signaling specificity and cell fate decision during stomatal development.

摘要

植物表皮上的气孔控制着气体和水分的交换,其形成依赖于 MAPK 相关过程。尽管 MAPK3(MPK3)和 MAPK6(MPK3/MPK6)对拟南芥气孔模式和分化的控制作用已经得到了广泛的研究,但它们是如何失活的以及如何调节不同阶段的气孔发育还不清楚。在这里,我们鉴定了一种双特异性磷酸酶,MAP KINASE PHOSPHATASE1(MKP1),它通过控制早期气孔发育过程中 MAPK 的激活,促进气孔细胞命运的转变。功能丧失会导致细胞簇形成,这些细胞无法分化成气孔,从而形成 pavement 细胞的斑块。我们表明,MKP1 在气孔信号通路中 YODA(MAPKKK)的下游但在 MPK3/MPK6 的上游起作用,并且 MKP1 缺陷导致体内气孔信号诱导的 MAPK 过度激活。通过在气孔谱系的三个离散细胞类型中表达 MKP1,我们进一步确定 MKP1 在早期气孔前体细胞中 MAPK 的失活介导了细胞命运的转变,从而导致气孔的分化。总之,我们的数据揭示了 MKP1 在控制 MAPK 信号特异性和气孔发育过程中细胞命运决定方面的重要作用。

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本文引用的文献

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Autocrine regulation of stomatal differentiation potential by EPF1 and ERECTA-LIKE1 ligand-receptor signaling.通过EPF1和类ERECTA1配体-受体信号传导对气孔分化潜能的自分泌调节
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Mitogen-Activated Protein Kinase Phosphatases Affect UV-B-Induced Stomatal Closure via Controlling NO in Guard Cells.丝裂原活化蛋白激酶磷酸酶通过控制保卫细胞中的一氧化氮来影响紫外线B诱导的气孔关闭。
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Phosphorylation and stabilization of Arabidopsis MAP kinase phosphatase 1 in response to UV-B stress.UV-B 胁迫下拟南芥 MAP 激酶磷酸酶 1 的磷酸化和稳定化。
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Arabidopsis MAP kinase phosphatase 1 and its target MAP kinases 3 and 6 antagonistically determine UV-B stress tolerance, independent of the UVR8 photoreceptor pathway.拟南芥丝裂原活化蛋白激酶磷酸酶 1 及其靶标丝裂原活化蛋白激酶 3 和 6 拮抗决定 UV-B 胁迫耐受性,独立于 UVR8 光受体途径。
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MAPK phosphatase AP2C3 induces ectopic proliferation of epidermal cells leading to stomata development in Arabidopsis.MAPK 磷酸酶 AP2C3 诱导表皮细胞异位增殖,导致拟南芥气孔发育。
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MAPK phosphatase MKP2 mediates disease responses in Arabidopsis and functionally interacts with MPK3 and MPK6.丝裂原活化蛋白激酶磷酸酶 MKP2 介导拟南芥的疾病反应,并与 MPK3 和 MPK6 具有功能相互作用。
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The Arabidopsis mitogen-activated protein kinase phosphatase PP2C5 affects seed germination, stomatal aperture, and abscisic acid-inducible gene expression.拟南芥丝裂原活化蛋白激酶磷酸酶 PP2C5 影响种子萌发、气孔开度和脱落酸诱导基因的表达。
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