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R C Sharma

Publications and source records attributed to R C Sharma.

At least 145 records · Page 8Linked to original sources
PubMed1987

Comparison of the rep-38 and mmrA1 mutations of Escherichia coli.

The rep-38 and mmrA1 mutations are located very close to each other (approximately 85 min), and have been suggested to be allelic. To address this question we have compared the phenotypes of the mmrA1 and rep-38 mutants. Both the mmrA1 and rep-38 mutations blocked the enhanced killing and inhibition of postreplication repair by rich growth medium that occurs in UV-irradiated Escherichia coli K-12 uvrA cells, i.e., the mmrA1 and rep-38 strains did not show minimal medium recovery (MMR). However, phi X174 bacteriophage propagated well in mmrA1 strains, but not in rep-38 strains; a rep mutation sensitized a uvrA strain to UV irradiation, but a mmrA mutation did not. During chloramphenicol treatment, the rep-38 strain showed a larger amount of residual DNA synthesis than observed in the mmrA1 strain. The mmrA1 mutation appears to be a dominant mutation. This was determined by the failure of either plasmid pLC44-7 or episome F'KLF11, both of which carry the mmrA+ gene, to complement the Mmr- phenotype of a uvrA mmrA strain. Plasmid pLC44-7 is known to complement the rep-38 mutation, suggesting that rep-38 is a recessive mutation. Although certain of the phenotypes of the rep and mmrA mutants are similar, a number are quite different. These differences suggest that these two mutations are not allelic.

Adenosine Triphosphatases↗
PubMed1987

A model for the recA-dependent repair of excision gaps in UV-irradiated Escherichia coli.

We have tested and supported the hypothesis that, in UV-irradiated Escherichia coli, recA-dependent nucleotide excision repair only functions in the replicated portion of the chromosome (i.e., where sister duplexes exist). Using a dnaA(Ts) mutation to align the chromosomes (i.e., all rounds of DNA replication were completed, and new rounds could not be initiated), we studied the genetic control of excision repair (measured as the repair of excision gaps in DNA) in cells with unreplicated chromosomes, and also in cells with partially replicated chromosomes. The excision repair that occurred in cells with unreplicated chromosomes was recA independent, but the excision repair that occurred in cells with partially replicated chromosomes was partially recA dependent. We found no evidence of interchromosomal recombination in recA-dependent excision repair. The majority of this recA-dependent excision repair was recF dependent, and a small portion was recB dependent. The recF and recB genes are suggested to function in excision repair in a manner similar to their function in postreplication repair, i.e., in the replicated portion of a chromosome, the RecF pathway repairs gaps, and the RecB pathway repairs the DNA double-strand breaks that arise at unrepaired gaps.

Chromosomes, Bacterial↗
PubMed1987

recA-dependent DNA repair in UV-irradiated Escherichia coli.

UV-radiation-induced lesions in DNA result in the formation of excision gaps, daughter-strand gaps (DSG) and double-strand breaks (DSB), which are repaired by several different mechanisms. Postreplication repair. The recA gene is a master gene that controls all of the pathways of postreplication repair. The repair of DSG proceeds by one pathway that is also recF dependent, and one pathway that is constitutive and independent of the recF and recBC genes. A small fraction of the recF recB-independent repair of DSG is dependent upon the umuC gene, and may define an error-prone pathway of postreplication repair. Unrepaired DSG can be converted to DSB, which are normally repaired by the RecBCD pathway. However, in the recBC sbcB background, these DSB are repaired by a recF-dependent process. The RecF pathways of postreplication repair appear to utilize DNA containing a single-stranded region (either a gap or a DSB with a single-stranded end), while the RecBCD pathway appears to utilize the blunt ends of duplex DNA to promote the recombinational repair of DSB. The polA gene (especially the 5'----3' exonuclease activity of DNA polymerase I) functions in pathways of postreplication repair (both for the repair of DSG and DSB) that are largely independent of the recF gene. Nucleotide excision repair. The repair of excision gaps is independent of the recA gene in cells with unreplicated chromosomes, but is recA dependent in cells with partially replicated chromosomes at the time of UV irradiation. This recA-dependent repair of excision gaps appears to be analogous to the recF- and recB-dependent pathways of postreplication repair, i.e. the RecF pathway repairs DNA gaps, and the RecBCD pathway repairs the DSB that arise at unrepaired gaps.

DNA Repair↗
PubMed1987

Role of DNA polymerase I in postreplication repair: a reexamination with Escherichia coli delta polA.

Using strains of Escherichia coli K-12 that are deleted for the polA gene, we have reexamined the role of DNA polymerase I (encoded by polA) in postreplication repair after UV irradiation. The polA deletion (in contrast to the polA1 mutation) made uvrA cells very sensitive to UV radiation; the UV radiation sensitivity of a uvrA delta polA strain was about the same as that of a uvrA recF strain, a strain known to be grossly deficient in postreplication repair. The delta polA mutation interacted synergistically with a recF mutation in UV radiation sensitization, suggesting that the polA gene functions in pathways of postreplication repair that are largely independent of the recF gene. When compared to a uvrA strain, a uvrA delta polA strain was deficient in the repair of DNA daughter strand gaps, but not as deficient as a uvrA recF strain. Introduction of the delta polA mutation into uvrA recF cells made them deficient in the repair of DNA double-strand breaks after UV irradiation. The UV radiation sensitivity of a uvrA polA546(Ts) strain (defective in the 5'----3' exonuclease of DNA polymerase I) determined at the restrictive temperature was very close to that of a uvrA delta polA strain. These results suggest a major role for the 5'----3' exonuclease activity of DNA polymerase I in postreplication repair, in the repair of both DNA daughter strand gaps and double-strand breaks.

Chloramphenicol↗
PubMed1987

Reversible sterility by cyproterone acetate plus testosterone enanthate in langur monkey with maintenance of libido.

Cyproterone acetate (1 mg/kg b.w. per day; oral) in combination with testosterone enanthate (2 mg/kg b.w. 15 days; i.m.) was administered for 60 and 90 days into adult male langur monkeys (Presbytis entellus entellus, Dufresne). Testicular weight and volume were reduced significantly. Spermatogenesis was suppressed but the interstitial cells appeared normal. Seminiferous tubules and Sertoli cell nuclear diameters were reduced significantly. The indices of testicular steroidogenesis, i.e. testicular total proteins, sialic acid, RNA and fructose showed a fall. On the contrary, cholesterol, total lipids, glycogen and phosphatases increased after treatment. Libido was not affected. Cessation of treatment resulted in a resumption of all the variables to normal levels within 90 days. The results reveal a reversible inhibition of testicular steroidogenesis which ultimately resulted in the disruption of spermatogenesis, a definite index of sterility. It is further emphasized that simultaneously administered testosterone enanthate maintains androgenicity.

Animals↗
PubMed1986

Testis functions and sexual potentia in langur monkey treated with a combination steroidal contraceptive formulation.

Administration of a combination formulation of danazol (100 mg/day; oral) plus testosterone enanthate (TE) (50 mg/15 days; i.m.) for 30 to 60 days in adult male langur monkeys resulted in the reversible suppression of testicular function without affecting the sexual potentia. Testicular weight and volume decreased significantly along with the mass atrophy of germinal epithelium and impaired morphology of Leydig and Sertoli cells. A conspicuous shrinkage of seminiferous tubules, Leydig cell nuclei and Sertoli cell nuclei was noted. Elevation of testicular cholesterol, total lipids, glycogen and phosphatases activity with the depletion of total proteins, nucleic acid, sialic acid and fructose was noteworthy. All changes were maintained during maintenance dose studies (danazol: 50 mg/day; oral plus TE: 50 mg/15 days; i.m.) for 60 days. Resumption of all measures to normal was evident following 120 days of recovery. It can be concluded that the exogenous TE substitutes the serum testosterone levels to maintain extratesticular androgen actions even after interference by danazol of Leydig cell function along with spermatogenesis inhibition.

Animals↗
PubMed1986

Repair of DNA double-strand breaks in UV-irradiated Escherichia coli uvrB recF cells is inhibited by rich growth medium.

Ultraviolet (UV)-irradiated uvrB recF and uvrB recB cells of Escherichia coli K-12 showed similar radiation sensitivities when plated on minimal growth medium (MM), however, the uvrB recF cells were much more UV radiation-sensitive than the uvrB recB cells when plated on rich growth medium. Sedimentation analysis of the DNA from UV-irradiated uvrB recF cells suggests that the rich medium killing of uvrB recF cells is due to the inhibition of the repair of UV-radiation-induced DNA double-strand breaks, i.e., the killing is due to the inhibition of the recB-dependent pathway of postreplication repair. Furthermore, we demonstrated that the DNA double-strand breaks that were formed in UV-irradiated uvrB recA200(Ts) cells incubated at 42 degrees C in rich growth medium were not repaired whether the medium during subsequent repair incubation at 30 degrees C was MM or rich growth medium, while DNA double-strand breaks that were formed in MM at 42 degrees C could be repaired in MM or in rich growth medium at 30 degrees C. How the absence of an abrupt slowing of DNA synthesis when UV-irradiated cells are held in rich growth medium (Sharma and Smith, 1985b) may prevent the repair of these DNA double-strand breaks is discussed.

Culture Media↗
PubMed1985

Changes in the biochemical composition of semen following danazol plus testosterone enanthate administration to the langur monkey.

Changes in the biochemical composition of semen, which reflect the accessory sex organ functions, following danazol (100 mg/day; orally) plus testosterone enanthate (50 mg/month; i.m.) administration have been investigated in langur monkey. The levels of acid phosphatase, lactic dehydrogenase and glycerylphosphorylcholine in the semen decreased significantly; whereas fructose, citric acid, magnesium and semen volume did not show any significant changes. A gradual decrease in the motility and count of spermatozoa was observed. At 60 days of treatment all animals became azoospermic. No drug related hematological changes were observed. The combination therapy impaired the epididymal and prostatic functions along with suppression of spermatogenesis.

Acid Phosphatase↗
PubMed1985

A minor pathway of postreplication repair in Escherichia coli is independent of the recB, recC and recF genes.

After ultraviolet (UV) irradiation, an Escherichia coli K12 uvrB5 recB21 recF143 strain (SR1203) was able to perform a limited amount of postreplication repair when incubated in minimal growth medium (MM), but not if incubated in a rich growth medium. Similarly, this strain showed a higher survival after UV irradiation if plated on MM versus rich growth medium (i.e., it showed minimal medium recovery (MMR]. In fact, its survival after UV irradiation on rich growth medium was similar to that of a uvrB5 recA56 strain, which does not show MMR or postreplication repair. The results obtained with a uvrB5 recF332::Tn3 delta recBC strain and a uvrB5 recF332::Tn3 recB21 recC22 strain were similar to those obtained for strain SR1203, suggesting that the recB21 and recF143 alleles are not leaky in strain SR1203. The treatment of UV-irradiated uvrB5 recB21 recF143 and uvrB5 recF332::Tn3 delta recBC cells with rifampicin for 2 h had no effect on survival or the repair of DNA daughter-strand gaps. Therefore, a pathway of postreplication repair has been demonstrated that is constitutive in nature, is inhibited by postirradiation incubation in rich growth medium, and does not require the recB, recC and recF gene products, which control the major pathways of postreplication repair.

Bacterial Proteins↗
PubMed1985

A mechanism for rich-medium inhibition of the repair of daughter-strand gaps in the deoxyribonucleic acid of UV-irradiated Escherichia coli K12 uvrA.

Ultraviolet-irradiated Escherichia coli K12 uvrA(B,C) cells show higher survival if plated on minimal growth medium (MM) rather than on rich growth medium (RM). This phenomenon has been referred to as 'minimal medium recovery' (MMR). UV-irradiated (4 J/m2) uvrA cells showed a similar rate of protein synthesis, whether incubated in MM or RM, however, they showed a severe depression in DNA synthesis when incubated in MM that lasted for about 30 min, and the normal rate of DNA synthesis was not reestablished until about 60 min after irradiation. When a sample of these same cells was switched to RM immediately after UV-irradiation, there was only a slight slowing of DNA synthesis, and the normal rate of synthesis was reestablished by 60 min. An additional mmrA mutation or growth retardation by valine blocked both this extra DNA synthesis in RM, and the inhibitory effect of RM on survival. These findings suggest that the absence of a marked delay in DNA synthesis observed in RM may be responsible for the inhibitory effect of RM on the survival of UV-irradiated excision-deficient cells. Two hypotheses, which are not mutually exclusive, are proposed and supported by data to explain why a fast rate of DNA synthesis after UV-irradiation partially inhibits postreplication repair and enhances cell lethality.

Bacterial Proteins↗
PubMed1985

An epidemiological study of 177 cases of human rabies.

Of the 177 rabies patients admitted to various hospitals in Amritsar city, 80.8% were males and 31.1% were children under the age of 15 years. Incidence was found to be gradually increasing in urban areas, although 68.2% were still found in rural areas. History of second or third degree bites existed in all the cases. Dogs were the source of exposure in 97.3% of cases and they were all suspected of having rabies. 49.1% of cases had bites on the lower extremities and 70.8% were on uncovered parts of the body. The incubation period was observed to be between 30 and 120 days in 61.8% of cases; 90.0% of the patients developed the disease within six months of exposure. Short incubation periods were observed in a majority of the patients bitten on more than one part of the body, head, neck and face or bitten on uncovered parts. Hydrophobia and death occurred in 100% of cases and 93.4% of patients died within five days. Post-exposure injections were reported in 10.2% of cases and these showed no definite incubation period pattern.

Adolescent↗