Azoulay-Shemer Tamar, Bagheri Andisheh, Wang Cun, Palomares Axxell, Stephan Aaron B, Kunz Hans-Henning, Schroeder Julian I
Division of Biological Sciences, Section of Cell and Developmental Biology, Center for Food and Fuel for the 21st Century, University of California, San Diego, La Jolla, California 92093-0116.
Division of Biological Sciences, Section of Cell and Developmental Biology, Center for Food and Fuel for the 21st Century, University of California, San Diego, La Jolla, California 92093-0116
Plant Physiol. 2016 Jun;171(2):788-98. doi: 10.1104/pp.15.01662. Epub 2016 Apr 21.
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.
淀粉代谢参与气孔运动调节。然而，淀粉缺陷型突变体是否影响二氧化碳诱导的气孔关闭，以及保卫细胞和/或叶肉细胞中的淀粉生物合成对于高二氧化碳诱导的气孔关闭是否具有限速作用，目前仍不清楚。在拟南芥（Arabidopsis thaliana）突变体中比较了气孔对[CO2]变化的响应和二氧化碳同化率，这些突变体要么在所有植物组织中都缺乏淀粉（ADP-葡萄糖焦磷酸化酶[ADGase]），要么在保卫细胞中保留淀粉积累，但在叶肉细胞中缺乏淀粉（质体磷酸葡萄糖异构酶[pPGI]）。ADGase突变体表现出二氧化碳诱导的气孔关闭受损，但pPGI突变体没有，这表明保卫细胞而非叶肉细胞中的淀粉生物合成在二氧化碳诱导的气孔关闭中起作用。尽管如此，淀粉缺陷型ADGase突变体等位基因表现出部分二氧化碳响应，表明存在一个可能由阴离子通道介导的与淀粉生物合成无关的响应成分。此外，当转移到高[CO2]时，ADGase和pPGI突变体的全叶二氧化碳同化率均降低，但只有ADGase突变体导致二氧化碳诱导的气孔关闭受损。这些遗传分析确定了淀粉生物合成在高二氧化碳诱导的气孔关闭中的作用。
