How environmental factors regulate mutagenesis and gene transfer in microorganisms

This review is focused on the physiological and evolutionary strategies of the processes occurring during the entry of microbial cells into stationary phase and the subsequent period of stasis. The molecular mechanisms adapting microorganisms from exponential growth to a static state involve activation and complex regulation of the stationary factor Sigma-S, which directs RNA polymerase to the specific promoters. As a result the static cells acquire general resistance (simultaneous tolerances) to different environmental stresses. In parallel with the physiological adaptation to stasis, diverse genetical processes are aimed towards resuming the growth of the static cells. Different types of mutagenesis occur: (i) in cells entering stasis and (ii) in static cells (adaptive mutagenesis). Cessation of growth induces the transient hypermutator state resulting in the accumulation of random mutations in the subpopulation of the static cells. If by chance, one or a few of such mutations lead to resumption of division, the growing cell will return to a normal mechanism of spontaneous mutagenesis. Another mechanism for generating genetical variability in stressed cells involves transposons and conjugative plasmids. Stresses can stimulate the excision of some transposons, which, in turn, can generate chromosomal mutations and activate intracellular mechanisms of mutagenesis. Under stress some conjugative plasmids activate genes encoding antirestriction proteins that repress restriction-modification systems of the recipient cells. Moreover, under stress special cellular mechanisms decrease (alleviate) the activity of restriction-modification systems which, in turn, enhance the probability of gene transfer into the stressed cells. Under stress, the efficiency of inter-species genetical barriers also decreases. This, stimulates inter-species gene transfer and may lead to a burst of incipient speciation in the population of non-growing cells. After resumption of growth the genetical barriers leading to isolation will be restored. In general, the cessation of growth “switches on”, and resumption of growth “switches off”, a set of special processes that are responsible for generating bursts of genetical variability in populations of microorganisms. This article is dedicated to the memory of Nikolai V Timofeev-Ressovsky (1900–1981).     

Genetical analysis of rifampicin resistant mutants of E. coli K 12

Summary E. coli rifampicin-resistant (rif-r) mutants were divided into two conventional groups: A, resistant to 50–100g/ml of rifampicin both on complete and minimal medium and B, sensitive to these concentrations of rifampicin on minimal, but resistant on complete medium. RNA polymerase from rif-r-A mutants is resistant to high concentrations of rifampicin in vitro while the enzyme from rif-r-B mutants but slightly if at all differs from the wild-type enzyme in its response to the drug.All rif-r-A and rif-r-B mutants are closely linked and map between argH and thi on E. coli K 12 chromosome. We failed to isolate any rifampicin-resistant mutants which would map outside this region.     

Prediction of the three-dimensional structure of aflatoxin of Aspergillus flavus by homology modelling

Aflatoxins are polyketide-derived secondary metabolites produced by Aspergillus spp. The toxic effects of aflatoxins have adverse consequences for human health and agricultural economics. The aflR gene, a regulatory gene for aflatoxin biosynthesis, encodes a protein containing a zinc-finger DNA-binding motif. AFLR-Protein three-dimensional model was generated using Robetta server. The modeled AFLR-Protein was further optimization and validation using Rampage. In the simulations, we monitored the backbone atoms and the C-α-helix of the modeled protein. The low RMSD and the simulation time indicate that, as expected, the 3D structural model of AFLR-protein represents a stable folding conformation. This study paves the way for generating computer molecular models for proteins whose crystal structures are not available and which would aid in detailed molecular mechanism of inhibition of aflatoxin.     

Will transgenic plants adversely affect the environment?

Transgenic insecticidal plants based onBacillus thuringiensis (Bt) endotoxins, on proteinase inhibitors and on lectins, and transgenic herbicide tolerant plants are widely used in modern agriculture. The results of the studies on likelihood and non-likelihood of adverse effects of transgenic plants on the environment including: (i) effects on nontarget species; (ii) invasiveness; (iii) potential for transgenes to ‘escape’ into the environment by horizontal gene transfer; and (iv) adverse effects on soil biota are reviewed. In general, it seems that large-scale implementation of transgenic insecticidal and herbicide tolerant plants do not display considerable negative effects on the environments and, moreover, at least some transgenic plants can improve the corresponding environments and human health because their production considerably reduces the load of chemical insecticides and herbicides.