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Journal of Bacteriology, November 2006, p. 7387-7395, Vol. 188, No. 21
0021-9193/06/$08.00+0 doi:10.1128/JB.00974-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.
,
Shigeki Ehira,2
Naoki Sato,3 and
C. Peter Wolk1,4*
MSU-DOE Plant Research Laboratory,1 Department of Plant Biology, Michigan State University, East Lansing, Michigan,4 Department of Biochemistry and Molecular Biology, Faculty of Science, Saitama University, Saitama, Japan,2 Department of Life Sciences, Graduate School of Arts and Sciences, University of Tokyo, Tokyo, Japan3
Received 4 July 2006/ Accepted 17 August 2006
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.
Published ahead of print on 25 August 2006.
Supplemental material for this article may be found at http://jb.asm.org/.
Present address: Northwestern University Feinberg School of Medicine, 303 East Chicago Avenue, Chicago, IL 60611-3008.
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