Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.23 (beta-galactosidase)
 14,648 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this paper we investigate how the inclusion of time delay alters the dynamical properties of the Jacob-Monod model, describing the control of the beta-galactosidase synthesis by the lac repressor protein in E. coli. The consequences of a time delay on the dynamics of this system are analysed using Hopf's theorem and Lyapunov-Andronov's theory applied to the original mathematical model and to an approximated version. Our analytical calculations predict that time delay acts as a key bifurcation parameter. This is confirmed by numerical simulations. A critical value of time delay, which depends on the values of the model parameters, is analytically established. Around this critical value, the properties of the system change drastically, allowing under certain conditions the emergence of stable limit cycles, that is self-sustained oscillations. In addition, the features of the end product repression play an essential role in the characterisation of these limit cycles: if cooperativity is considered in the end product repression, time delay higher than the mentioned critical value induce differentiated responses during the oscillations, provoking cycles of all-or-nothing response in the concentration of the species.
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PMID:Dynamic properties of a delayed protein cross talk model. 1770 75

The mce2 operon is one of the four mce operons present in Mycobacterium tuberculosis that encode exported proteins with a probable role in the virulence mechanisms of this bacterium. In the present study we demonstrated that Rv0586, which encodes a putative GntR-like regulator, is part of the mce2 operon. By using a promoter-lacZ fusion approach and bioinformatics tools, we found that Rv0586 represses the expression of Mce2 proteins and of a putative endonuclease IV, encoded by end (Rv0670) gene. For this reason, we have re-named the repressor protein Mce2R. By gel-shift experiments Mce2R binding was determined to be located within the mce2 promoter region. In addition, two FadR-like operator motifs were identified within the promoter regions of both the mce2 operon and the end gene. These motifs overlap putative -10 and -35 promoter boxes. M. tuberculosis carrying mce2 and end promoter-lacZ fusions were used to infect J774 macrophage-like cells. Expression of beta-galactosidase was induced after phagocytocis, suggesting that some cellular factor could be a key component of the molecular switch regulation expression of the mce2 operon. In conclusion, these results add novel evidence of the complex regulation of mce operon expression.
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PMID:Mce2R from Mycobacterium tuberculosis represses the expression of the mce2 operon. 1902 63


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