Molecular characterization of catabolite repression by succinate in the nodulating bacterium Sinorhizobium meliloti Page: 1 of 7
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Final Report (7/26/2006)
Covering 9/2001 to 5/2006
DE-FG02-01ER15175 "Molecular characterization of catabolite repression by succinate in
the nodulating bacterium Sinorhizobium meliloti" PI: Daniel J. Gage, University of
Connecticut, Dept. of Molecular and Cell Biology
Our initial Energy Biosciences grant from the DOE, was designed to generate information into how
the progress of succinate-mediated catabolite repression (SMCR) operates in the nitrogen-fixing
symbiont Sinorhizobium meliloti. The rational for studying catabolite repression in S. meliloti was
twofold. First, the genes and proteins that affect catabolite repression are often extremely important
in controlling processes that are among the most fundamental in bacteria. These include control of
central metabolic pathways, and control of growth, cell division and differentiation. Secondly, S.
meliloti offered a unique opportunity to gain insight into catabolite repression in response to
succinate and other dicarboxylic acids. While, catabolite repression in response to compounds like
succinate had been documented in several important groups of bacteria, the molecular mechanisms
involved in its operation were obscure. Because most work done on catabolite repression involved
organisms that preferred glucose and related sugars, we anticipated that study of succinate-
mediated catabolite repression in S. meliloti would lead to unique insights into the molecular
physiology of this organism, and perhaps lead to insights into the metabolic, and gene-regulatory
affairs of other organisms that use TCA-cycle intermediates as preferred carbon sources.
In order to better understand SMCR in S. meliloti we proposed the following two specific aims:
A. To characterize the succinate-repressed promoter region of melA using biochemical and
B. To identify S. meliloti genes needed to establish succinate mediated repression.
The progress we made on these two aims is described below:
A. Characterization of the succinate-repressed promoter region of melA using biochemical
and genetic approaches.
We had shown, before submission of the original DOE proposal, that S. meliloti has an operon
encoding an a-galactosidase and four proteins that make up a periplasmic-binding-protein
dependent ABC a-galactoside transport system. We had shown that these genes were required for
the uptake and utilization of a-galactosides such as melibiose, raffinose and stachyose. We had also
shown that the expression of these genes is repressed by succinate, even when inducers such as
melibiose or raffinose are present. It was this operon (the melA-agp = melibiase, a-gal transport)
that we suggested would make a good model for studying SMCR. The following was
accomplished terms of characterizing this operon in terms of its induction by a-galactosides and
repression by succinate.
1. We showed that the melA-agp operon requires an AraC-type transcriptional activator for
induction. This gene encoding this activator, agpT, is immediately upstream melA and is
transcribed in the opposite direction. Mutation of agpT results in cells that are unable to grow on a-
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Gage, Daniel. Molecular characterization of catabolite repression by succinate in the nodulating bacterium Sinorhizobium meliloti, report, September 27, 2006; United States. (digital.library.unt.edu/ark:/67531/metadc881860/m1/1/: accessed November 20, 2018), University of North Texas Libraries, Digital Library, digital.library.unt.edu; crediting UNT Libraries Government Documents Department.