Data from: Arabidopsis MKK10-MPK6 mediates red-light-regulated opening of seedling cotyledons through phosphorylation of PIF3

Photomorphogenesis is an important process in which seedlings emerge from soil and begin autotrophic growth. Photomorphogenesis mechanisms include light signal perception, signal transduction, and the modulation of light-responsive genes expression, ultimately leading to cellular and developmental changes. Phytochrome-interacting factors (PIFs) play pivotal roles in negatively regulating photomorphogenesis. Light-induced activation of phytochromes triggers the rapid phosphorylation and degradation of PIFs, but the kinases responsible for the phosphorylation of PIFs are largely unknown. Here, we show that Arabidopsis MPK6 is a kinase involved in phosphorylating PIF3 and regulating red (R) light-induced cotyledon opening, a crucial process during seedling photomorphogenesis. MPK6 was activated by R light, and cotyledon opening angle in R light was reduced in mpk6 seedlings. MKK10, a MAPKK whose function is currently unclear, appears to act as a kinase upstream of MPK6 in regulating cotyledon opening. The activation of MPK6 by MKK10 led to the phosphorylation of PIF3 and accelerated its turnover in transgenic seedlings. Accordingly, the overexpression of PIF3 suppressed the MKK10-induced cotyledon opening. MKK10-MPK6 function downstream of phyB in regulating seedlings cotyledon opening in R light. Therefore, MKK10-MPK6 cascade appears to mediate the regulation of R light-controlled seedling photomorphogenesis,via a mechanism that might involve the phosphorylation of PIF3.光形态建成（Photomorphogenesis）是幼苗破土而出并启动自养生长的重要生理过程。其调控机制涵盖光信号感知、信号转导以及光响应基因表达调控，最终引发细胞与发育层面的一系列变化。光敏色素互作因子（Phytochrome-interacting factors, PIFs）在负调控光形态建成中发挥关键作用。光诱导的光敏色素活化会触发PIFs的快速磷酸化与降解，但迄今尚未明确负责催化PIFs磷酸化的激酶种类。本研究发现，拟南芥MPK6作为一种激酶，可参与磷酸化PIF3并调控红光（R光）诱导的子叶张开——这是幼苗光形态建成过程中的关键环节。MPK6可被R光激活，且mpk6突变体幼苗在R光下的子叶张开角度显著降低。MKK10作为一种功能尚不明确的促分裂原活化蛋白激酶激酶（MAPKK），似乎在调控子叶张开的通路中作为MPK6的上游激酶发挥作用。MKK10对MPK6的活化可引发PIF3的磷酸化，并加速其在转基因幼苗中的周转降解。相应地，PIF3的过表达会抑制MKK10诱导的子叶张开表型。在R光调控幼苗子叶张开的过程中，MKK10-MPK6级联反应作用于光敏色素B（phyB）的下游。综上，MKK10-MPK6级联反应似乎通过磷酸化PIF3的分子机制，介导了R光调控的幼苗光形态建成过程。