Academic literature on the topic 'Rifampicin‐resistant Mutants'
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Journal articles on the topic "Rifampicin‐resistant Mutants"
Al- Khafaji, K. A., and A. N. Al- Thwami. "Identification of differences in virulence factors production from mutant isolates of clinical Vibrio cholerae S." Journal of Biotechnology Research Center 5, no. 1 (January 1, 2011): 61–73. http://dx.doi.org/10.24126/jobrc.2011.5.1.149.
Full textOstash, B. O., Yu Misaki, B. S. Dolya, Ya I. Kharaton, T. Busche, A. M. Luzhetskyy, J. Kalinowski, K. Ochi, and V. O. Fedorenko. "Generation and initial characterization of a collection of spontaneous Streptomyces albus J1074 mutants resistant to rifampicin." Faktori eksperimental'noi evolucii organizmiv 27 (September 1, 2020): 139–43. http://dx.doi.org/10.7124/feeo.v27.1316.
Full textJin, Ding Jun, William A. Walter, and Carol A. Gross. "Characterization of the termination phenotypes of rifampicin-resistant mutants." Journal of Molecular Biology 202, no. 2 (July 1988): 245–53. http://dx.doi.org/10.1016/0022-2836(88)90455-x.
Full textLee, D. H., R. J. Miles, and J. R. M. Inal. "Antibiotic sensitivity and mutation rates to antibiotic resistance inMycoplasma mycoidesssp.mycoides." Epidemiology and Infection 98, no. 3 (June 1987): 361–68. http://dx.doi.org/10.1017/s0950268800062129.
Full textBhatnagar, N., E. Getachew, S. Straley, J. Williams, M. Meltzer, and A. Fortier. "Reduced Virulence Of Rifampicin-Resistant Mutants Of Francisella Tularensis [X]." Journal of Infectious Diseases 170, no. 4 (October 1, 1994): 841–47. http://dx.doi.org/10.1093/infdis/170.4.841.
Full textDo, Thi Thuy, Jerónimo Rodríguez-Beltran, Esmeralda Cebrián-Sastre, Alexandro Rodríguez-Rojas, Alfredo Castañeda-García, and Jesús Blázquez. "Inactivation of a New Potassium Channel Increases Rifampicin Resistance and Induces Collateral Sensitivity to Hydrophilic Antibiotics in Mycobacterium smegmatis." Antibiotics 11, no. 4 (April 12, 2022): 509. http://dx.doi.org/10.3390/antibiotics11040509.
Full textSeverinov, K., M. Soushko, A. Goldfarb, and V. Nikiforov. "Rifampicin region revisited. New rifampicin-resistant and streptolydigin-resistant mutants in the beta subunit of Escherichia coli RNA polymerase." Journal of Biological Chemistry 268, no. 20 (July 1993): 14820–25. http://dx.doi.org/10.1016/s0021-9258(18)82407-3.
Full textRodriguez, Carlos Hernan, Alejandra De Ambrosio, Milena Bajuk, Mariela Spinozzi, Marcela Nastro, Karina Bombicino, Marcela Radice, Gabriel Gutkind, Carlos Vay, and Angela Famiglietti. "In vitro antimicrobials activity against endemic Acinetobacter baumannii multiresistant clones." Journal of Infection in Developing Countries 4, no. 03 (February 3, 2010): 164–67. http://dx.doi.org/10.3855/jidc.604.
Full textvon Freiesleben, Ulrik, Knud V. Rasmussen, Tove Atlung, and Flemming G. Hansen. "Rifampicin-resistant initiation of chromosome replication from oriC in ihf mutants." Molecular Microbiology 37, no. 5 (September 2000): 1087–93. http://dx.doi.org/10.1046/j.1365-2958.2000.02060.x.
Full textSilvia, Sophia, Samantha A. Donahue, Erin E. Killeavy, Gerwald Jogl, and Steven T. Gregory. "A Survey of Spontaneous Antibiotic-Resistant Mutants of the Halophilic, Thermophilic Bacterium Rhodothermus marinus." Antibiotics 10, no. 11 (November 11, 2021): 1384. http://dx.doi.org/10.3390/antibiotics10111384.
Full textDissertations / Theses on the topic "Rifampicin‐resistant Mutants"
Reinders, Svenja. "Do rifampicin-resistant mutants modulate RpoS regulation of gene expression?" Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-123718.
Full textWillemse, Danicke. "Regulation of efflux in rifampicin resistant mutants of Mycobacterium tuberculosis." Thesis, Stellenbosch : Stellenbosch University, 2013. http://hdl.handle.net/10019.1/79820.
Full textENGLISH ABSTRACT: Multidrug resistant tuberculosis (MDR-TB), defined as having resistance to at least the first-line drugs, isoniazid and rifampicin (RIF), is a global health problem. Mutations in the rpoB gene, encoding the β-subunit of RNA polymerase, are implicated in RIF resistance - with the S531L and H526Y mutations occurring most frequently. The level of RIF resistance varies for strains with identical rpoB mutations, which suggests that other factors play a role in RIF resistance. Efflux has been implicated in determining the intrinsic level of RIF resistance. Increased expression of the multidrug efflux pump, Rv1258c, following RIF exposure was observed in some Mycobacterium tuberculosis MDR clinical isolates and H37Rv RIF mono-resistant mutants, but not others. The factors influencing the induction of Rv1258c are poorly understood. The aim of this study was to investigate the effects of rpoB mutations on expression of Rv1258c and whiB7, a transcriptional regulator of Rv1258c, in M. tuberculosis H37Rv in vitro generated RIF resistant mutants, in the absence and presence of RIF. The promoter region of M. tuberculosis H37Rv Rv1258c was cloned into a position upstream of a lacZ gene (encoding β-galactosidase) in multi-copy episomal and integrating vectors. Vector functioning and the effect of rpoB mutations on Rv1258c promoter activity were initially investigated in the non-pathogenic related species, Mycobacterium smegmatis mc2155 rpoB mutants and subsequently in M. tuberculosis by doing β-galactosidase assays. qRT-PCR was done to investigate the effects of rpoB mutations on native Rv1258c and whiB7 gene expression. Episomal and integrating vectors were functional and the integrating vector system was used for subsequent β-galactosidase assays in M. tuberculosis. Rv1258c promoter activity in the S531L mutant was approximately 1.5 times less and in the H526Y mutant 1.5 times higher than that of the wild-type in M. smegmatis. Similarly, Rv1258c promoter activity in the S531L mutant was approximately half and in the H526Y mutant approximately double that of the wild-type in M. tuberculosis. A similar trend in Rv1258c and whiB7 expression to those observed using β-galactosidase assays were observed when investigating the native Rv1258c and whiB7 gene transcript levels compared to the wild-type using qRT-PCR, although differences were not significant. Exposure of the M. smegmatis and M. tuberculosis rpoB mutants to sub-inhibitory levels of RIF did not affect Rv1258c promoter activity. Mutations in rpoB had a marginal effect on Rv1258c and whiB7 transcript levels, but showed the same trend as that seen for Rv1258c promoter activity. It remains to be determined whether these differences are biologically significant. When considering efflux pumps as new targets for treatment, possible differences in efflux pumps expression due to different rpoB mutations should be considered.
AFRIKAANSE OPSOMMING: Multi-middel weerstandige tuberkulose (MDR-TB) word gedefinieer as weerstandigheid tot ten minste rifampisien (RIF) en isoniasied, wat deel van die eerstelyn anti-tuberkulose behandeling vorm. Mutasies in die rpoB geen, wat die β-subeenheid van die RNA polimerase enkodeer, word geassosieer met RIF weerstandigheid. S531L en H526Y rpoB mutasies kom die algemeenste voor. RIF weerstandigheids vlakke verskil egter tussen isolate met identiese rpoB mutasies, wat impliseer dat ander faktore ook 'n rol in RIF weerstandigheid speel. 'n Toename in transkripsie van die Rv1258c geen, wat 'n multi-middel effluks pomp enkodeer, is waargeneem met blootstelling aan RIF, slegs in sommige M. tuberculosis H37Rv RIF mono-weerstandige mutante and MDR kliniese isolate, maar nie in ander nie. Die faktore wat die induksie van die Rv1258c effluks pomp beïnvloed is nie goed nagevors nie. Die studie ondersoek die effek van die rpoB mutasies op die uitdrukking van die Rv1258c en whiB7,'n transkripsionele regulator van Rv1258c, gene in M. tuberculosis H37Rv in vitro gegenereerde RIF weerstandige mutante, in die teenwoordigheid en afwesigheid van RIF. Die promotor area van die M. tuberculosis H37Rv Rv1258c geen is in 'n posisie stroomop van 'n lacZ geen, wat vir β-galaktosidase enkodeer, in multi-kopie episomale en integreerende vektors ingekloneer. Die funksionaliteit van die vektor en effek van rpoB mutasies op Rv1258c promotor aktiwiteit is ondersoek in die naverwante nie-patogeniese spesies, M. smegmatis en daarna in M. tuberculosis deur β-galaktosidase essais te doen. qRT-PCR is gedoen om die effek van rpoB mutasies op die vlak van transkripsie van die natuurlike Rv1258c geen en die whiB7 geen te bestudeer. Beide die episomale en integreerende vektors was funksioneel en daar is besluit om die integreerende vektor vir daaropeenvolgende β-galaktosidase essais in M. tuberculosis te gebruik. Rv1258c promotor aktiwiteit van die S531L mutant was ongeveer 1.5 keer minder as en die van die H526Y mutant 1.5 keer hoër as die van die ongemuteerde bakterië in M. smegmatis. Soortgelyk was die Rv1258c promoter aktiwiteit van die S531L mutant ongeveer die helfde van en die van H526Y mutant ongeveer dubbel die van die ongemuteerde bakterië in M. tuberculosis 'n Soortgelyke neiging in die vlakke van Rv1258c en whiB7 transkripte van die natuurlike geen is gedurende qRT-PCR waargeneem alhoewel die verskille nie beduidend was nie. Blootstelling aan sub-inhibitoriese konsentrasies van RIF het geen effek op Rv1258c uitdrukking in die M. smegmatis of M. tuberculosis rpoB mutante gehad nie. Die rpoB mutasies het net 'n effense effek op Rv1258c en whiB7 transkrip vlakke in M. tuberculosis rpoB mutante, maar transkrip vlakke het 'n soortgelyke neiging as die Rv1258c promoter aktiwiteit getoon. Of die waargenome verskille biologies betekenisvol is, moet nog bepaal word. Indien effluks pompe as teikens vir bahandeling gebruik sou word, moet in ag geneem word dat effluks pompe moontlik verskillend uitgedruk word in verskillende rpoB mutante.
The DST/NRF Centre of Excellence in Biomedical Tuberculosis Research, Stellenbosch University
DAAD-NRF in Country Scholarship and Ernst and Ethel Eriksen Trust
Harry Crossley Foundation
Sharmada, S. "Cellular and Molecular Features of the Response of Mycobacterium smegmatis to Rifampicin and Moxifloxacin Upon Prolonged Exposure." Thesis, 2017. http://etd.iisc.ac.in/handle/2005/4168.
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