Lechno-Yossef Sigal, Fan Qing, Ehira Shigeki, Sato Naoki, Wolk C Peter
MSU-DOE Plant Research Laboratory, Michigan State University, East Lansing, 48824-1312, USA.
J Bacteriol. 2006 Nov;188(21):7387-95. doi: 10.1128/JB.00974-06. Epub 2006 Aug 25.
Regulatory genes hepK, hepN, henR, and hepS are required for heterocyst maturation in Anabaena sp. strain PCC 7120. They presumptively encode two histidine kinases, a response regulator, and a serine/threonine kinase, respectively. To identify relationships between those genes, we compared global patterns of gene expression, at 14 h after nitrogen step-down, in corresponding mutants and in the wild-type strain. Heterocyst envelopes of mutants affected in any of those genes lack a homogeneous, polysaccharide layer. Those of a henR mutant also lack a glycolipid layer. patA, which encodes a positive effector of heterocyst differentiation, was up-regulated in all mutants except the hepK mutant, suggesting that patA expression may be inhibited by products related to heterocyst development. hepS and hepK were up-regulated if mutated and so appear to be negatively autoregulated. HepS and HenR regulated a common set of genes and so appear to belong to one regulatory system. Some nontranscriptional mechanism may account for the observation that henR mutants lack, and hepS mutants possess, a glycolipid layer, even though both mutations down-regulated genes involved in formation of the glycolipid layer. HepK and HepN also affected transcription of a common set of genes and therefore appear to share a regulatory pathway. However, the transcript abundance of other genes differed very significantly from expression in the wild-type strain in either the hepK or hepN mutant while differing very little from wild-type expression in the other of those two mutants. Therefore, hepK and hepN appear to participate also in separate pathways.
调控基因hepK、hepN、henR和hepS是鱼腥藻PCC 7120菌株异形胞成熟所必需的。据推测,它们分别编码两种组氨酸激酶、一种应答调节因子和一种丝氨酸/苏氨酸激酶。为了确定这些基因之间的关系,我们比较了氮饥饿14小时后相应突变体和野生型菌株中基因表达的整体模式。在这些基因中任何一个受到影响的突变体的异形胞包膜都缺乏均匀的多糖层。henR突变体的异形胞包膜也缺乏糖脂层。编码异形胞分化正效应因子的patA在除hepK突变体之外的所有突变体中均上调,这表明patA的表达可能受到与异形胞发育相关产物的抑制。hepS和hepK发生突变时会上调,因此似乎存在负自调控。HepS和HenR调控一组共同的基因,因此似乎属于一个调控系统。尽管henR突变体缺乏而hepS突变体具有糖脂层这一现象是由下调参与糖脂层形成的基因导致的,但某些非转录机制可能对此做出了解释。HepK和HepN也影响一组共同基因的转录,因此似乎共享一条调控途径。然而,在hepK或hepN突变体中,其他基因的转录本丰度与野生型菌株中的表达差异非常显著,而在这两个突变体中的另一个中与野生型表达的差异则很小。因此,hepK和hepN似乎也参与了不同的途径。