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Iron deficiency ends up into several unavoidable consequences including damaging oxidative stress in cyanobacteria. NtcA is a global nitrogen regulator controls wide range of metabolisms in addition to regulation of nitrogen metabolism. In present communication, NtcA based regulation of iron homeostasis, ROS production and cellular phenotype under iron deficiency in Anabaena 7120 has been investigated. NtcA regulates the concentration dependent iron uptake by controlling the expression of furA gene. NtcA also regulated pigment synthesis and phenotypic alterations in Anabaena 7120. A significant increase in ROS production and corresponding reduction in the activities of antioxidative enzymes (SOD, CAT, APX and GR) in CSE2 mutant strain in contrast to wild type Anabaena 7120 also suggested the possible involvement of NtcA in protection against oxidative stress in iron deficiency. NtcA has no impact on the expression of furB and furC in spite of presence of consensus NtcA binding site (NBS) and ?10 boxes in their promoter. NtcA also regulates the thylakoid arrangement as well as related photosynthetic and respiration rates under iron deficiency in Anabaena 7120. Overall results suggested that NtcA regulates iron acquisition and in turn protect Anabaena cells from the damaging effects of oxidative stress induced under iron deficiency.  相似文献   

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Sato H  Fujimori T  Sonoike K 《FEBS letters》2008,582(7):1093-1096
The sll1961 gene was reported to encode a regulatory factor of photosystem stoichiometry in the cyanobacterium Synechocystis sp. PCC 6803. We here show that the sll1961 gene is also essential for the phycobilisome degradation during nitrogen starvation. The defect in phycobilisome degradation was observed in the sll1961 mutant despite the increased expression of nblA, a gene involved in phycobilisome degradation during nitrogen starvation. Photosystem stoichiometry is not affected by nitrogen starvation in the sll1961 mutant nor in the wild-type. The results indicate the presence of a novel pathway for phycobilisome degradation control independent of nblA expression.  相似文献   

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拟南芥SEN1基因受衰老诱导.将该基因启动子融合报告基因萄聚糖酶(glucuronidase,GUS)基因转入拟南芥,通过染色并测定GUS活性发现,缺氮、缺磷、缺钾诱导叶中SEN1表达,而只有缺磷能导根中SEN1表达.缺磷对根叶中SEN1的诱导被3%葡萄糖和细胞分裂素抑制.3%葡萄糖胺在根和叶中均诱导SEN1表达,外源细胞分裂素不能抑制这种效应.结果表明:SEN1基因可受缺磷信号特异调控,并受糖信号和细胞分裂素负调控;葡萄糖胺能大大促进根和叶中SEN1表达,且不受细胞分裂素的负调控.  相似文献   

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