A recombination-deficient (Rec-) strain of Caulobacter crescentus has been isolated from a collection of mutants sensitive to ultraviolet irradiation. The Rec- mutant fails to give recombinants following phi Cr30-mediated generalized transduction or following RP4-mediated conjugation. The recombination frequency in the Rec- strain is at least 5000-fold lower than in the wild type strains. The Rec- mutant is indistinguishable from wild type in terms of morphology, growth rate, viability, and phage sensitivities, differing only in properties known to be associated with recA-type mutations in other organisms: recombination frequency, ultraviolet sensitivity, and Weigle reactivation. The map location of the rec-526 allele has not been identified, but rec-526 can be cotransferred with the fla-169 mutation by RP4-mediated conjugation at low frequency. This apparent linkage has been used to move the rec mutation to other strains. The Rec- mutant resembles recA strains of other organisms and provides a healthy strain severely deficient in recombination for use in complementation and cloning studies involving C. crescentus.
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http://dx.doi.org/10.1007/BF00383006 | DOI Listing |
The centromere effect (CE) is a meiotic phenomenon that ensures meiotic crossover suppression in pericentromeric regions. Despite being a critical safeguard against nondisjunction, the mechanisms behind the CE remain unknown. Previous studies have shown that various regions of the pericentromere, encompassing proximal euchromatin, beta and alpha heterochromatin, undergo varying levels of crossover suppression, raising the question of whether distinct mechanisms establish the CE in these different regions.
View Article and Find Full Text PDFBr J Cancer
December 2024
Institute of Clinical Sciences, Imperial College London, London, UK.
Background: Quiescence is reversible proliferative arrest. Multiple mechanisms regulate quiescence that are not fully understood. High expression of the CDK inhibitor p21 correlates with a poor prognosis in non-small cell lung cancer (NSCLC) and, in non-transformed cells, p21 promotes quiescence after replication stress.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Biomedical Sciences and Biomedical Engineering, Faculty of Medicine, Prince of Songkla University, Songkhla 90110, Thailand.
Engineered interleukin-18 (IL-18) has attracted interest as a cytokine-based treatment. However, knowledge-based mutagenesis of IL-18 has been reported for only a few regions of the protein structures, including binding sites I and II. When coupled with the binding region mutant (E6K), the non-binding residue of IL-18, Thr63 (T63), has been shown to increase the flexibility of the binding loop.
View Article and Find Full Text PDFNeurol Sci
December 2024
Department of Molecular Medicine, Faculty of Medicine and Cardiovascular Diseases Research Center, Birjand University of Medical Sciences, Birjand, Iran.
Introduction: Galloway-Mowat syndrome type 3 (GAMOS3) is a rare genetic disorder with renal and neurological complications caused by pathogenic variants in the OSGEP gene. Here, we report the molecular basis and clinical features in an Iranian family.
Methods: Our proband, a 10-month-old female patient, presented with microcephaly, global developmental delay, lower limb spasticity, facial dysmorphisms, and renal tubulopathy.
BMC Med Genomics
November 2024
Department of Medical Genetics, School of Advanced Technologies in Medicine, Golestan University of Medical Sciences, Gorgan, Iran.
Background: Hearing Loss (HL) is the most common sensorineural condition in humans. Mutations in the TMPRSS3 gene (DNFB8/10 locus) have been linked to autosomal recessive non-syndromic hearing loss (ARNSHL).
Methods: Whole-exome sequencing (WES) was utilized to identify disease-causing variants in a proband from Iran with ARNSHL who presented clinically with sensorineural, bilateral, and prelingual HL.
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