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Starch Biosynthesis in Guard Cells But Not in Mesophyll Cells Is Involved in CO2-Induced Stomatal Closing

机译:保护细胞中而不是叶肉细胞中的淀粉生物合成涉及CO2诱导的气孔关闭

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摘要

Starch metabolism is involved in stomatal movement regulation. However, it remains unknown whether starch-deficient mutants affect CO2-induced stomatal closing and whether starch biosynthesis in guard cells and/or mesophyll cells is rate limiting for high CO2-induced stomatal closing. Stomatal responses to [CO2] shifts and CO2 assimilation rates were compared in Arabidopsis (Arabidopsis thaliana) mutants that were either starch deficient in all plant tissues (ADP-Glc-pyrophosphorylase [ADGase]) or retain starch accumulation in guard cells but are starch deficient in mesophyll cells (plastidial phosphoglucose isomerase [pPGI]). ADGase mutants exhibited impaired CO2-induced stomatal closure, but pPGI mutants did not, showing that starch biosynthesis in guard cells but not mesophyll functions in CO2-induced stomatal closing. Nevertheless, starch-deficient ADGase mutant alleles exhibited partial CO2 responses, pointing toward a starch biosynthesis-independent component of the response that is likely mediated by anion channels. Furthermore, whole-leaf CO2 assimilation rates of both ADGase and pPGI mutants were lower upon shifts to high [CO2], but only ADGase mutants caused impairments in CO2-induced stomatal closing. These genetic analyses determine the roles of starch biosynthesis for high CO2-induced stomatal closing.
机译:淀粉代谢参与气孔运动调节。然而,尚不清楚淀粉缺乏的突变体是否影响CO 2诱导的气孔关闭,以及保卫细胞和/或叶肉细胞中淀粉的生物合成是否对高CO 2诱导的气孔关闭具有速率限制。在拟南芥(Arabidopsis thaliana)突变体中比较了气孔对[CO2]转变和CO2同化率的响应,这些突变体在所有植物组织中均缺乏淀粉(ADP-Glc-焦磷酸化酶[ADGase]),或在保卫细胞中保留了淀粉积累,但淀粉缺乏在叶肉细胞中(质体磷酸葡萄糖异构酶[pPGI])。 ADGase突变体表现出受损的CO2诱导的气孔关闭,但pPGI突变体没有,表明守卫细胞中的淀粉生物合成,但在CO2诱导的气孔关闭中没有叶肉功能。然而,缺乏淀粉的ADGase突变体等位基因表现出部分CO 2响应,指向响应可能由阴离子通道介导的淀粉生物合成非依赖性成分。此外,ADGase和pPGI突变体的全叶CO2同化率在转换为高[CO2]时较低,但只有ADGase突变体会导致CO2诱导的气孔关闭受损。这些遗传分析确定了淀粉生物合成对高CO 2诱导的气孔关闭的作用。

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