Nonspecific inhibition of proline dehydrogenase synthesis in Escherichia coli during osmotic stress.
Nonspecific inhibition of proline dehydrogenase synthesis in Escherichia coli during osmotic stress.
复制标题
渗透胁迫期间大肠杆菌脯氨酸脱氢酶合成的非特异性抑制。
DOI:
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发表时间:
1989
期刊:
影响因子:
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通讯作者:
V. J. Stone
中科院分区:
文献类型:
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作者:
C. Deutch;J. M. Hasler;R. M. Houston;M. Sharma;V. J. Stone
L-Proline, which is accumulated by Escherichia coli during growth in media of high osmolality, also induces the synthesis of the enzyme degrading it to glutamate. To determine if proline catabolism is inhibited during osmotic stress, proline utilization and the formation of proline dehydrogenase were examined in varying concentrations of NaCl and sucrose. Although the specific growth rate of E. coli with proline as the sole nitrogen source diminished as the solute osmolality increased, a comparable reduction in growth rate occurred with ammonium as the primary nitrogen source. Proline catabolism, as measured in whole cells by the conversion of [14C]proline to [14C]glutamate, was only slightly inhibited by solute osmolalities up to 1.0 osmol/kg; more than 50% of the initial activity was still found at 2.0 osmol/kg. By contrast, the specific activity of proline dehydrogenase in bacteria grown in the presence of added solutes decreased to less than 20% of the control level. This reduction was related to a lower rate of synthesis, but was independent of genes currently known to be involved in osmoregulation or proline metabolism. The specific activities of tryptophanase, beta-galactosidase, and histidinol dehydrogenase were also reduced under similar growth conditions. These results indicate that while proline catabolism is not directly inhibited by high solute concentrations, prolonged exposure to osmotic stress leads to its reduction as part of a more general metabolic response.
DOI:
10.1073/pnas.78.1.464
发表时间:
1981-01-01
期刊:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子:
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作者:
LAIMINS, LA;RHOADS, DB;EPSTEIN, W
通讯作者:
EPSTEIN, W