MAPK phosphatase AP2C3 induces ectopic proliferation of epidermal cells leading to stomata development in Arabidopsis.
MAPK phosphatase AP2C3 induces ectopic proliferation of epidermal cells leading to stomata development in Arabidopsis.
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DOI：
10.1371/journal.pone.0015357
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发表时间：
2010-12-23
期刊：
影响因子：
3.7
通讯作者：
Meskiene I
中科院分区：
文献类型：
--
作者：
Umbrasaite J;Schweighofer A;Kazanaviciute V;Magyar Z;Ayatollahi Z;Unterwurzacher V;Choopayak C;Boniecka J;Murray JA;Bogre L;Meskiene I
在植物胚胎后表皮中，丝裂原激活蛋白激酶 (MAPK) 信号传导促进铺面细胞的分化并抑制气孔的形成。气孔是专门调节气体交换和水分流失的细胞。拟南芥 MAPK MPK3 和 MPK6 是信号级联的核心；然而，目前尚不清楚这些多效性 MAPK 的活性如何在空间上受到限制，从而仅在气孔谱系之外促进路面细胞分化。在这里，我们鉴定了一种称为 AP2C3（拟南芥蛋白磷酸酶 2C）的 PP2C 型磷酸酶，它在气孔发育过程中独特表达，并与 MPK3、MPK4 和 MPK6 相互作用并使其失活。 AP2C3 与细胞核内的 MAPK 共定位，这种定位取决于其 N 末端延伸。我们发现其他密切相关的磷酸酶 AP2C2 和 AP2C4 也是作用于 MPK6 的 MAPK 磷酸酶，但具有与 AP2C3 不同的表达模式。据此，只有 AP2C3 异位表达才能刺激细胞增殖，导致气孔过度发育。 AP2C3 的这一功能依赖于 MAPK 对接和细胞内定位所需的域。与此同时，组成型和诱导型 AP2C3 表达解除了 E2F-RB 通路的调节，促进 CDKA 的丰度和活性，以及 CDKB1;1 形式的变化。我们认为 AP2C3 下调 MAPK 信号活性，以帮助维持气孔和路面细胞分化之间的平衡。
In plant post-embryonic epidermis mitogen-activated protein kinase (MAPK) signaling promotes differentiation of pavement cells and inhibits initiation of stomata. Stomata are cells specialized to modulate gas exchange and water loss. Arabidopsis MAPKs MPK3 and MPK6 are at the core of the signaling cascade; however, it is not well understood how the activity of these pleiotropic MAPKs is constrained spatially so that pavement cell differentiation is promoted only outside the stomata lineage. Here we identified a PP2C-type phosphatase termed AP2C3 (Arabidopsis protein phosphatase 2C) that is expressed distinctively during stomata development as well as interacts and inactivates MPK3, MPK4 and MPK6. AP2C3 co-localizes with MAPKs within the nucleus and this localization depends on its N-terminal extension. We show that other closely related phosphatases AP2C2 and AP2C4 are also MAPK phosphatases acting on MPK6, but have a distinct expression pattern from AP2C3. In accordance with this, only AP2C3 ectopic expression is able to stimulate cell proliferation leading to excess stomata development. This function of AP2C3 relies on the domains required for MAPK docking and intracellular localization. Concomitantly, the constitutive and inducible AP2C3 expression deregulates E2F-RB pathway, promotes the abundance and activity of CDKA, as well as changes of CDKB1;1 forms. We suggest that AP2C3 downregulates the MAPK signaling activity to help maintain the balance between differentiation of stomata and pavement cells.
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