Affiliation:
1. Departments of Biochemistry and Developmental Biology, Stanford University School of Medicine, Stanford, California
Abstract
ABSTRACT
Insertion of an internal DNA fragment into the
act1
gene, which encodes one of several ς
54
-activator proteins in
Myxococcus xanthus
, produced a mutant defective in fruiting body development. While fruiting-body aggregation appears normal in the mutant, it fails to sporulate (<10
−6
the wild-type number of viable spores). The A and C intercellular signals, which are required for sporulation, are produced by the mutant. But, while it produces A-factor at levels as high as that of the wild type, the mutant produces much less C-signal than normal, as measured either by C-factor bioassay or by the total amount of C-factor protein detected with specific antibody. Expression of three C-factor-dependent reporters is altered in the mutant: the level of expression of Ω4414 is about 15% of normal, and Ω4459 and Ω4403 have alterations in their time course. Finally, the methylation of FrzCD protein is below normal in the mutant. It is proposed that Act1 protein responds to C-signal reception by increasing the expression of the
csgA
gene. This C-signal-dependent increase constitutes a positive feedback in the wild type. The
act1
mutant, unable to raise the level of
csgA
expression, carries out only those developmental steps for which a low level of C-signaling is adequate.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Cited by
28 articles.
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