首页> 外文期刊>FEBS Letters >Starch biosynthesis by AGPase, but not starch degradation by BAM1/3 and SEX1, is rate‐limiting for CO2‐regulated stomatal movements under short‐day conditions
【24h】

Starch biosynthesis by AGPase, but not starch degradation by BAM1/3 and SEX1, is rate‐limiting for CO2‐regulated stomatal movements under short‐day conditions

机译:AGPase的淀粉生物合成,但BAM1 / 3和SEX1不能降解淀粉,是短期条件下CO2调节气孔运动的速率限制。

获取原文
           

摘要

Starch in guard cells functions in osmoregulation during stomatal movements. Starch metabolism is controlled by the circadian clock. We investigated the role of starch metabolism in stomatal responses to CO2 under different photoperiodic conditions. Guard cell starch levels correlate with low/high [CO2] exposure. Starch biosynthesis‐deficient AGPase (ADG1) mutants but, unexpectedly, not the starch degradation‐deficient BAM1, BAM3, and SEX1 mutants alone, are rate‐limiting for stomatal conductance responses to [CO2]‐shifts. Interestingly, AGPase is rate‐limiting solely under short‐ but not long‐day conditions. These findings suggest a model of enhanced AGPase activity in guard cells under short days such that starch biosynthesis becomes rate‐limiting for CO2‐induced stomatal closing.
机译:保卫细胞中的淀粉在气孔运动期间在渗透调节中起作用。淀粉代谢受生物钟控制。我们调查了淀粉代谢在不同光周期条件下气孔对CO2响应中的作用。保卫细胞淀粉水平与低/高[CO2]暴露量相关。淀粉生物合成缺陷型AGPase(ADG1)突变体,但并非仅淀粉降解缺陷型BAM1,BAM3和SEX1突变体,对气孔电导对[CO2]位移的响应具有速率限制。有趣的是,AGPase仅在短期而不是长期的情况下进行限速。这些发现表明,在短时间内,保卫细胞中AGPase活性增强的模型使得淀粉的生物合成成为限制CO2诱导的气孔关闭的速率。

著录项

相似文献

  • 外文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号