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聚球藻PCC 7942氮调节蛋白PipX在NtcA调控过程中的作用。

Role of the Synechococcus PCC 7942 nitrogen regulator protein PipX in NtcA-controlled processes.

作者信息

Espinosa Javier, Forchhammer Karl, Contreras Asunción

机构信息

División de Genética, Universidad de Alicante, Apartado 99, E-03080 Alicante, Spain.

Institut für Mikrobiologie und Molekularbiologie, Universität Giessen, Heinrich-Buff-Ring 26-32, D-35392 Giessen, Germany.

出版信息

Microbiology (Reading). 2007 Mar;153(Pt 3):711-718. doi: 10.1099/mic.0.2006/003574-0.

DOI:10.1099/mic.0.2006/003574-0
PMID:17322191
Abstract

The Synechococcus sp. PCC 7942 nitrogen regulator PipX interacts in a 2-oxoglutarate-dependent manner with the global nitrogen transcription factor NtcA and the signal transduction protein P(II). In vivo, PipX is involved in the NtcA-dependent induction of glnB and glnN genes. To further investigate the extent to which PipX is involved in global nitrogen control, the effect of pipX inactivation on various nitrogen-regulated processes was determined. The PipX-deficient mutant was able to use nitrate as a nitrogen source and to efficiently inhibit the nitrate transport upon ammonium addition but showed decreased nitrate and nitrite reductase activities and a delay in the induction of nitrate utilization after transfer of cultures from ammonium- to nitrate-containing media. In contrast to the wild-type, glutamine synthetase activity was not upregulated upon depletion of combined nitrogen from cultures of the mutant strain. Inactivation of pipX impaired induction of nblA and delayed phycobilisome degradation, but did not affect recovery of nitrogen-deprived cultures. Taken together, the results indicate that PipX interacts with NtcA to facilitate efficient acclimation of cyanobacteria to conditions of nitrogen limitation.

摘要

聚球藻属PCC 7942氮调节因子PipX以依赖于2-氧代戊二酸的方式与全局氮转录因子NtcA和信号转导蛋白P(II)相互作用。在体内,PipX参与NtcA依赖的glnB和glnN基因的诱导。为了进一步研究PipX参与全局氮控制的程度,确定了pipX失活对各种氮调节过程的影响。PipX缺陷型突变体能够利用硝酸盐作为氮源,并在添加铵后有效抑制硝酸盐转运,但显示出硝酸盐和亚硝酸盐还原酶活性降低,以及在培养物从含铵培养基转移到含硝酸盐培养基后硝酸盐利用诱导延迟。与野生型相比,突变株培养物中结合态氮耗尽后,谷氨酰胺合成酶活性未上调。pipX失活损害了nblA的诱导并延迟了藻胆体降解,但不影响缺氮培养物的恢复。综上所述,结果表明PipX与NtcA相互作用,以促进蓝藻对氮限制条件的有效适应。

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