Expression of maize calcium‐dependent protein kinase (ZmCPK11) improves salt tolerance in transgenic Arabidopsis plants by regulating sodium and potassium homeostasis and stabilizing photosystem II

脱落酸 光系统II 拟南芥 茉莉酸 生物 转基因作物 转基因 盐度 细胞生物学 植物 光合作用 生物化学 基因 生态学 突变体
作者
Lidia Borkiewicz,Lidia Polkowska‐Kowalczyk,Jarosław Cieśla,Paweł Sowiński,Maciej Jończyk,Wojciech Rymaszewski,Katarzyna Patrycja Szymańska,Radosław Jaźwiec,Grażyna Muszyńska,Jadwiga Szczegielniak
出处
期刊:Physiologia Plantarum [Wiley]
卷期号:168 (1): 38-57 被引量:32
标识
DOI:10.1111/ppl.12938
摘要

In plants, CALCIUM-DEPENDENT PROTEIN KINASES (CDPKs/CPKs) are involved in calcium signaling in response to endogenous and environmental stimuli. Here, we report that ZmCPK11, one of maize CDPKs, participates in salt stress response and tolerance. Salt stress induced expression and upregulated the activity of ZmCPK11 in maize roots and leaves. Activation of ZmCPK11 upon salt stress was also observed in roots and leaves of transgenic Arabidopsis plants expressing ZmCPK11. The transgenic plants showed a long-root phenotype under control conditions and a short-root phenotype under NaCl, abscisic acid (ABA) or jasmonic acid (JA) treatment. Analysis of ABA and JA content in roots indicated that ZmCPK11 can mediate root growth by regulating the levels of these phytohormones. Moreover, 4-week-old transgenic plants were more tolerant to salinity than the wild-type plants. Their leaves were less chlorotic and showed weaker symptoms of senescence accompanied by higher chlorophyll content and higher quantum efficiency of photosystem II. The expression of Na+ /K+ transporters (HKT1, SOS1 and NHX1) and transcription factors (CBF1, CBF2, CBF3, ZAT6 and ZAT10) with known links to salinity tolerance was upregulated in roots of the transgenic plants upon salt stress. Furthermore, the transgenic plants accumulated less Na+ in roots and leaves under salinity, and showed a higher K+ /Na+ ratio in leaves. These results show that the improved salt tolerance in ZmCPK11-transgenic plants could be due to an upregulation of genes involved in the maintenance of intracellular Na+ and K+ homeostasis and a protection of photosystem II against damage.

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