To optimize growth and development, plants monitor photosynthetic activities and appropriately regulate various cellular processes. However, signaling mechanisms that coordinate plant growth with photosynthesis remain poorly understood. To identify factors that are involved in signaling related to photosynthetic stimuli, we performed a phosphoproteomic analysis with Marchantia polymorpha, an extant bryophyte species in the basal lineage of land plants. Among proteins whose phosphorylation status changed differentially between dark-treated plants and those after light irradiation, but failed to do so in the presence of a photosynthesis inhibitor, we identified a B4-group Raf-like kinase, named PHOTOSYNTHESIS-RELATED RAF (MpPRAF). Biochemical analyses confirmed photosynthesis-activity-dependent changes in the phosphorylation status of MpPRAF. Mutations in the MpPRAF gene resulted in growth retardation. Measurement of carbohydrates demonstrated both hyper-accumulation of starch and reduction of sucrose in Mppraf mutants. Neither inhibition of starch synthesis nor exogenous supply of sucrose alleviated the growth defect, suggesting serious impairment of Mppraf mutants in both the synthesis of sucrose and the repression of its catabolism. As a result of the compromised photosynthate metabolism, photosynthetic electron transport was down-regulated in Mppraf mutants. A mutated MpPRAF with a common amino-acid substitution for inactivating kinase activity was unable to rescue the Mppraf mutant defects. Our results provide evidence that MpPRAF is a photosynthesis signaling kinase that regulates sucrose metabolism.

中文翻译：

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通过Raf-like激酶在多形草多形花March中对光合碳水化合物代谢的调节。

为了优化生长和发育，植物监测光合作用活动并适当调节各种细胞过程。然而，协调植物生长与光合作用的信号传导机制仍然知之甚少。为了确定与光合作用刺激相关的信号传导所涉及的因素，我们用陆地植物基础谱系中现存的苔藓植物种类的多形花March进行了蛋白质组学分析。在蛋白质的磷酸化状态在黑暗处理过的植物和光照后的植物之间存在差异，但在光合作用抑制剂的作用下未能做到这一点，我们鉴定出一种B4基团Raf样激酶，称为光合作用相关的RAF（MpPRAF） 。生化分析证实了MpPRAF磷酸化状态的光合作用活性依赖性变化。MpPRAF基因的突变导致生长迟缓。碳水化合物的测量证明了Mppraf突变体中淀粉的过度积累和蔗糖的减少。淀粉合成的抑制或蔗糖的外源供应均不能缓解生长缺陷，这表明Mppraf突变体在蔗糖的合成及其分解代谢的抑制中均受到严重损害。由于光合产物代谢受损，Mppraf突变体中的光合电子传递被下调。具有用于失活激酶活性的常见氨基酸取代的突变MpPRAF无法挽救Mppraf突变体缺陷。我们的结果提供了证据，表明MpPRAF是调节蔗糖代谢的光合作用信号激酶。碳水化合物的测量证明了Mppraf突变体中淀粉的过度积累和蔗糖的减少。淀粉合成的抑制或蔗糖的外源供应均不能缓解生长缺陷，这表明Mppraf突变体在蔗糖的合成及其分解代谢的抑制中均受到严重损害。由于光合产物代谢受损，Mppraf突变体中的光合电子传递被下调。具有用于失活激酶活性的常见氨基酸取代的突变MpPRAF无法挽救Mppraf突变体缺陷。我们的结果提供了证据，表明MpPRAF是调节蔗糖代谢的光合作用信号激酶。碳水化合物的测量证明了Mppraf突变体中淀粉的过度积累和蔗糖的减少。淀粉合成的抑制或蔗糖的外源供应均不能缓解生长缺陷，这表明Mppraf突变体在蔗糖的合成及其分解代谢的抑制中均受到严重损害。由于光合产物代谢受损，Mppraf突变体中的光合电子传递被下调。具有用于失活激酶活性的常见氨基酸取代的突变MpPRAF无法挽救Mppraf突变体缺陷。我们的结果提供了证据，表明MpPRAF是调节蔗糖代谢的光合作用信号激酶。淀粉合成的抑制或蔗糖的外源供应均不能缓解生长缺陷，这表明Mppraf突变体在蔗糖的合成及其分解代谢的抑制中均受到严重损害。由于光合产物代谢受损，Mppraf突变体中的光合电子传递被下调。具有用于失活激酶活性的常见氨基酸取代的突变MpPRAF无法挽救Mppraf突变体缺陷。我们的结果提供了证据，表明MpPRAF是调节蔗糖代谢的光合作用信号激酶。淀粉合成的抑制或蔗糖的外源供应均不能缓解生长缺陷，这表明Mppraf突变体在蔗糖的合成及其分解代谢的抑制中均受到严重损害。由于光合产物代谢受损，Mppraf突变体中的光合电子传递被下调。具有用于失活激酶活性的常见氨基酸取代的突变MpPRAF无法挽救Mppraf突变体缺陷。我们的结果提供了证据，表明MpPRAF是调节蔗糖代谢的光合作用信号激酶。Mppraf突变体中光合电子传递被下调。具有用于失活激酶活性的常见氨基酸取代的突变MpPRAF无法挽救Mppraf突变体缺陷。我们的结果提供了证据，表明MpPRAF是调节蔗糖代谢的光合作用信号激酶。Mppraf突变体中光合电子传递被下调。具有用于失活激酶活性的常见氨基酸取代的突变MpPRAF无法挽救Mppraf突变体缺陷。我们的结果提供了证据，表明MpPRAF是调节蔗糖代谢的光合作用信号激酶。