scholarly journals NtrX systemically controls transcription of the CtrA system genes to regulate Rhizobium cell division

2020 ◽  
Author(s):  
Shenghui Xing ◽  
Fang An ◽  
Xinwei Yang ◽  
Leqi Huang ◽  
Shuang Zeng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Signaling Pathway ◽  
Cell Cycle Regulation ◽  
Response Regulator ◽  
Transcriptional Level ◽  
Dna Interactions ◽  
Nitrogen Response ◽  
Nutrient Response ◽  
Protein Dna Interactions ◽  
Cycle Regulation

AbstractIn α-proteobacteria, the CtrA signaling pathway regulates cell cycle progression. A species whose cell duplication is associated with CtrA stability is affected by the response regulator NtrX. However, the function of NtrX acting on the cell cycle regulation in bacteria remains unclear. Here, we report that NtrX controls transcription of the CtrA system genes involved in cell cycle regulation in a legume symbiont, Sinorhizobium meliloti. Three groups of ntrX mutants showed the similar cell cycle defects, such as slow growth, abnormal shapes, and irregular genomic DNA accumulation. Expression of the CtrA signaling pathway genes including ctrA, gcrA, dnaA, divL and cpdR1, is differentially regulated by the phosphorylated NtrX protein. The regulation is achieved through direct protein-DNA interactions. The 53rd aspartate residue known as the conserved phosporylation site and located in the receiver domain of NtrX, is required for S. meliloti cell cycle regulation. Interestingly, expression of S. meliloti ntrX derivatives in Caulobacter and Agrobacterium strains showed distinct defects of cell duplication and growth, suggesting that NtrX plays different roles in cell cycle regulation in these bacteria. Our findings demonstrate that NtrX is an upstream transcriptional regulator of the CtrA signaling pathway in S. meliloti, which could be associated with nitrogen nutrient response.Author SummaryCell cycle regulation in alpha-proteobacteria is dictated by the conserved CtrA signaling pathway. Transcription of the CtrA system genes is mainly regulated by CtrA and GcrA. CcrM, SciP and MucR also participate in transcription regulation of ctrA. However, the regulation by a nutrient response regulator at transcriptional level remains unclear. Here, we report that the nitrogen response regulator, NtrX systemically regulates transcription of several CtrA system genes by protein-DNA interactions in a legume symbiont, S. meliloti. The similar mechanism is proposed in the pathogens of Agrobacterium and Brucella species. These findings provide a new prospect to understand the hierarchy of transcriptional regulation in a bacterial cell cycle.

scholarly journals The Rb-CDK4/6 Signaling Pathway Is Critical in Neural Precursor Cell Cycle Regulation

2000 ◽  
Vol 275 (43) ◽  
pp. 33593-33600 ◽  
Author(s):  
Kerry L. Ferguson ◽  
Steven M. Callaghan ◽  
Michael J. O'Hare ◽  
David S. Park ◽  
Ruth S. Slack
Keyword(s):  
Cell Cycle ◽  
Signaling Pathway ◽  
Cell Cycle Regulation ◽  
Precursor Cell ◽  
Neural Precursor ◽  
Neural Precursor Cell ◽  
Cycle Regulation

scholarly journals Cell cycle-regulated transcription of the CLB2 gene is dependent on Mcm1 and a ternary complex factor.

1995 ◽  
Vol 15 (6) ◽  
pp. 3129-3137 ◽  
Author(s):  
M Maher ◽  
F Cong ◽  
D Kindelberger ◽  
K Nasmyth ◽  
S Dalton
Keyword(s):  
Cell Cycle ◽  
Dna Binding ◽  
Cell Cycle Regulation ◽  
Ternary Complex ◽  
Binding Activity ◽  
Transcriptional Level ◽  
Dna Binding Activity ◽  
Cycle Regulation ◽  
Ternary Complex Factor

Clb2 is the major B-type mitotic cyclin required for entry into mitosis in the budding yeast Saccharomyces cerevisiae. We showed that accumulation of CLB2 transcripts in G2 cells is controlled at the transcriptional level and identified a 55-bp upstream activating sequence (UAS) containing an Mcm1 binding site as being necessary and sufficient for cell cycle regulation. Sequences within the cell cycle-regulated UAS were shown to bind Mcm1 in vitro, and mutation which abolished Mcm1-dependent DNA binding activity eliminated cell cycle-regulated transcription in vivo. A second protein with no autonomous DNA binding activity was also recruited into Mcm1-UAS complexes, generating a ternary complex. A point mutation in the CLB2 UAS which blocked ternary complex formation, but still allowed Mcm1 to bind, resulted in loss of cell cycle regulation in vivo, suggesting that the ternary complex factor is also important in control of CLB2 transcription. We discuss the possibility that the CLB2 gene is coregulated with other genes known to be regulated with the same periodicity and suggest that Mcm1 and the ternary complex factor may coordinately regulate several other G2-regulated transcripts.

scholarly journals Cyclophosphamide Inhibits PI3K/AKT/mTOR Signaling Pathway in Mice Kidneys

Proceedings ◽  
2018 ◽  
Vol 2 (25) ◽  
pp. 1587 ◽  
Author(s):  
Gulsah Albayrak ◽  
Pinar Kilicarslan Sonmez ◽  
Damla Akogullari ◽  
Elgin Turkoz Uluer
Keyword(s):  
Cell Cycle ◽  
Protein Synthesis ◽  
Signaling Pathway ◽  
Cell Cycle Regulation ◽  
Kidney Tissue ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Cellular Functions ◽  
Cycle Regulation ◽  
Experimental Group

Cyclophosphamide (CTX), also known as cytophosphane among other, is a medication used as chemotherapy and to suppress the immune system. The PI3K/AKT/mTOR pathway is involved in the regulation of diverse cellular functions, including cell growth, protein synthesis, cell cycle regulation, glucose metabolism, and motility. In our study eight weeks old C57BL/6 female mice were divided into 3 groups as control (C), sham (S) and experimental group. The experimental group has been established with CTX treatment. No treatment was applied to the C group. The S group were given an equal amount of saline. CTX was administered intraperitoneally one every 2 days for 3 weeks; the first dose was 70 mg/kg, the ongoing doses were 30 mg/kg. At the end of 3 weeks mice were sacrificed and kidneys were taken for investigation. In order to show the effect of cyclophosphamide in kidney tissue, the tissues were stained via indirect immunohistochemistry with PI3K, AKT and mTOR primary antibodies. In our study, PI3K, AKT and mTOR expression levels were found to be significantly decreased in CTX-mediated mechanisms indicating that the mechanisms of CTX might involve in the inhibition of PI3K/AKT/mTOR signaling pathway.

scholarly journals Micro-ribonucleic acid and carcinogenesis: breast cancer as an example

2015 ◽  
Author(s):  
Manal Al-Khanbashi ◽  
Mansour Al-Moundhri
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Cycle ◽  
Ribonucleic Acid ◽  
Cell Cycle Regulation ◽  
Potential Role ◽  
Disease Status ◽  
Transcriptional Level ◽  
Non Coding Rnas ◽  
Cycle Regulation

MicroRNAs (miRNAs) are a class of small non-coding RNAs that have unique functions at post-transcriptional level (epigenetics). MiRNAs play a pivotal role in controlling gene expression at various levels including differentiation, cell-cycle regulation, apoptosis and many others in mammals as well as in many organisms. Recently, there has been greater understanding of the contribution of dysregulation of miRNA into disease status in particular carcinogenesis. In this review, we will discuss miRNA discovery, nomenclature, function, contribution of their dysregulation into disease status in particular carcinogenesis and their potential role as biomarkers.

Activating E2Fs mediate transcriptional regulation of human E2F6 repressor

2006 ◽  
Vol 290 (1) ◽  
pp. C189-C199 ◽  
Author(s):  
Tarrah E. Lyons ◽  
Maysoon Salih ◽  
Balwant S. Tuana
Keyword(s):  
Cell Cycle ◽  
Binding Sites ◽  
Cell Cycle Regulation ◽  
Promoter Activity ◽  
Time Course ◽  
Family Members ◽  
Ectopic Expression ◽  
Transcriptional Level ◽  
Mrna Levels ◽  
Cycle Regulation

E2F6 is believed to repress E2F-responsive genes and therefore serve a role in cell cycle regulation. Analysis of the human E2F6 promoter region revealed the presence of two putative E2F binding sites, both of which were found to be functionally critical because deletion or mutations of these sites abolished promoter activity. Ectopic expression of E2F1 protein was found to increase E2F6 mRNA levels and significantly upregulate E2F6 promoter activity. Deletion or mutation of the putative E2F binding sites nullified the effects of E2F1 on the E2F6 promoter activity. Studies on the temporal induction of E2F family members demonstrated that the activating E2Fs, and most notably E2F1, were upregulated before E2F6 during cell cycle progression at the G1/S phase, and this coincided with the time course of induction experienced by the E2F6 promoter during the course of the cell cycle. EMSAs indicated the specific binding of nuclear complexes to the E2F6 promoter that contained E2F1-related species whose binding was specifically competed by the consensus E2F binding site. Chromatin immunoprecipitation assays with anti-E2Fs demonstrated the association of E2F family members with the E2F6 promoter in vivo. These data indicate that the expression of the E2F6 repressor is influenced at the transcriptional level by E2F family members and suggest that interplay among these transcriptional regulators, especially E2F1, may be critical for cell cycle regulation.

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