A new insight into RecA filament regulation by RecX from the analysis of conformation-specific interactions.

RecA protein mediates homologous recombination repair in bacteria through assembly of long helical filaments on ssDNA in an ATP-dependent manner. RecX, an important negative regulator of RecA, is known to inhibit RecA activity by stimulating the disassembly of RecA nucleoprotein filaments. Here we use a single-molecule approach to address the regulation of () RecA-ssDNA filaments by RecX () within the framework of distinct conformational states of RecA-ssDNA filament.

Single-Molecule Insights into ATP-Dependent Conformational Dynamics of Nucleoprotein Filaments of RecA.

(Dr) has one of the most robust DNA repair systems, which is capable of withstanding extreme doses of ionizing radiation and other sources of DNA damage. DrRecA, a central enzyme of recombinational DNA repair, is essential for extreme radioresistance. In the presence of ATP, DrRecA forms nucleoprotein filaments on DNA, similar to other bacterial RecA and eukaryotic DNA strand exchange proteins.

Deinococcus radiodurans RecA nucleoprotein filaments characterized at the single-molecule level with optical tweezers.

Deinococcus radiodurans can survive extreme doses of ionizing radiation due to the very efficient DNA repair mechanisms that are able to cope even with hundreds of double-strand breaks. RecA, the critical protein of homologous recombination in bacteria, is one of the key components of the DNA-repair system. Repair of double-strand breaks requires RecA binding to DNA and assembly of the RecA nucleoprotein helical filaments.

[The place and significance of the autonomic dystonia syndrome in the clinico-pathophysiological structure of the late sequelae of mild closed craniocerebral trauma].

Analysis of the incidence, clinico-pathophysiological structure and dynamics of vegetovascular disorders in subjects with a history of mild closed craniocerebral injuries has demonstrated that in the majority of them, even practically healthy, functional insufficiency of vegetovascular functions is seen for many years after injury. Clinically, it manifests under the influence of diverse harmful exo- and endogenous factors, undergoes circadian changes, is altered during magnetic storms, in the course of traumatic disease and nonmedicamentous correction (by methods of adaptive bioregulation according to heart rhythm parameters, craniocerebral hypothermia, etc). It has been shown that initially transitory, reversible vegetovascular disturbances, provided they were not initially removed, transform with years to more stable vegetotrophic disorders and become risk factor of cerebrovascular diseases in the given group.

[Late sequelae of mild closed cranio-cerebral injuries (incidence, clinical course and criteria of the conditions of compensation and decompensation)].

The authors present the results of clinical catamnestic, clinical neurologic analysis, and of specific neurophysiologic examinations of 292 patients with a history of slight craniocerebral injuries. Late sequelae of these injuries were detected in 70% of the examinees. The criteria and factors of decompensation risk were defined on the basis of the total and clinical structure of the disease, history of the injury, variation pulsometry, bioelectric reactivity, and visual analyzer adaptation function.