The Glycosyltransferase QUA1 Regulates Chloroplast-Associated Calcium Signaling During Salt and Drought Stress in Arabidopsis.
The Glycosyltransferase QUA1 Regulates Chloroplast-Associated Calcium Signaling During Salt and Drought Stress in Arabidopsis.
复制标题
糖基转移酶 QUA1 在拟南芥盐胁迫和干旱胁迫期间调节叶绿体相关的钙信号传导。
DOI：
10.1093/pcp/pcw192
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发表时间：
2017
期刊：
影响因子：
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通讯作者：
Guo Yan
中科院分区：
文献类型：
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作者：
Zheng Yuan;Liao Chancan;Zhao Shuangshuang;Wang Chongwu;Guo Yan
各种信号诱导的细胞质Ca2+([Ca2+]cyt)升高负责适当的下游反应。通过对胁迫诱导的[Ca2+]细胞化缺陷拟南芥突变体的遗传筛选，糖基转移酶QUASIMODO1 （QUA1）被鉴定为[Ca2+]细胞素对盐胁迫反应的调节因子。与野生型相比，在NaCl处理下，qua1-4突变体的[Ca2+]细胞显著增加。功能分析表明，QUA1是一种新的叶绿体蛋白，调节细胞质Ca2+信号。在叶绿体类囊体中检测到QUA1， QUA1 -4突变体呈现不规则堆积的颗粒。在qua1-4突变体中，叶绿体功能恢复后，[Ca2+]细胞的增加被抑制。进一步分析发现，类囊体定位钙传感器CAS也显示出不规则堆积的颗粒，并且qua1-4双突变体的叶绿体与CAS -1植株相似。在过表达qua1的植物中，CAS蛋白水平降低，且在渗透胁迫下易于降解。当在qua1-4突变体中沉默encas时，大量的[Ca2+]细胞增加被阻断，plc3和plc4的高表达被抑制。在渗透胁迫下，qua1-4突变体的[Ca2+]细胞水平甚至更高，并且对干旱胁迫敏感。然而，当qua1-4突变体中[Ca2+]细胞的增加受到抑制时，这种敏感性受到抑制。总的来说，我们的数据表明，在盐和干旱胁迫下，QUA1可能在叶绿体依赖的钙信号传导中起作用。此外，CAS可能在QUA1的下游发挥作用，介导这些过程。
Cytoplasmic Ca2+([Ca2+]cyt) elevation induced by various signals is responsible for appropriate downstream responses. Through a genetic screen ofArabidopsis thalianamutants defective in stress-induced [Ca2+]cytelevation, the glycosyltransferase QUASIMODO1 (QUA1) was identified as a regulator of [Ca2+]cytin response to salt stress. Compared with the wild type, thequa1-4mutant exhibited a dramatically greater increase in [Ca2+]cytunder NaCl treatment. Functional analysis showed that QUA1 is a novel chloroplast protein that regulates cytoplasmic Ca2+signaling. QUA1 was detected in chloroplast thylakoids, and thequa1-4mutant exhibited irregularly stacked grana. The observed greater increase in [Ca2+]cytwas inhibited upon recovery of chloroplast function in thequa1-4mutant. Further analysis showed that CAS, a thylakoid-localized calcium sensor, also displayed irregularly stacked grana, and the chloroplasts of thequa1-4 cas-1double mutant were similar to those ofcas-1plants. In QUA1-overexpressing plants, the protein level of CAS was decreased, and CAS was readily degraded under osmotic stress. WhenCASwas silenced in thequa1-4mutant, the large [Ca2+]cytincrease was blocked, and the higher expression ofPLC3andPLC4was suppressed. Under osmotic stress, thequa1-4mutant showed an even greater elevation in [Ca2+]cytand was hypersensitive to drought stress. However, this sensitivity was inhibited when the increase in [Ca2+]cytwas repressed in thequa1-4mutant. Collectively, our data indicate that QUA1 may function in chloroplast-dependent calcium signaling under salt and drought stresses. Additionally, CAS may function downstream of QUA1 to mediate these processes.