AI Article Synopsis
- Septin 7 (SEPT7) is crucial for completing cell division in mouse fibroblasts; its absence leads to multinucleated cells that cannot proliferate.
- Researchers created a model using Sept7-deficient fibroblasts that allowed for the reintroduction of normal SEPT7 through a doxycycline-inducible system.
- Analysis of SEPT7 mutants showed that while they had distinct biochemical properties, all successfully restored proper cell division, suggesting that SEPT7's ability to form specific filaments isn't essential for cytokinesis.
Article Abstract
Septin 7 (SEPT7) has been described to be essential for successful completion of cytokinesis in mouse fibroblasts, and Sept7-deficiency in fibroblasts constitutively results in multinucleated cells which stop proliferation. Using Sept7(flox/flox)fibroblasts we generated a cellular system, where the cytokinetic defects of Cre-mediated deletion of the Sept7 gene can be rescued by ectopically expressed doxycycline-inducible wild type SEPT7. Using this system, we analyzed the ability of SEPT7-mutants with alterations in their GTPase domain-dependent dimerization to prevent multinucleation and rescue proliferation. Although biochemical analysis of the mutants demonstrates differences in homo- and/or hetero-polymerization, in GTP-binding and/or GTPase activities, all analyzed mutants were able to rescue the cytokinesis phenotype of Sept7(flox/flox)fibroblasts associated with Cre-mediated deletion of endogenous Sept7. These findings indicate that the ability of septins to assemble into well-defined SEPT7-dimerization dependent native filaments is dispensable for cytokinesis in fibroblasts and opens the way to search for other mechanisms of the involvement of SEPT7 in cytokinesis.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4730212 | PMC |
| http://dx.doi.org/10.1038/srep20007 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
X-Ray Fluoroscopy-Based Kinematic Analysis of Quadrupedal Locomotion in Slow and Fast Fatigue-Resistant Motor Neuron-Deleted Mice.
Muscle Nerve
February 2025
Department of Mechanical Engineering, Faculty of Science and Technology, Keio University, Yokohama, Kanagawa, Japan.
Introduction/aims: VAChT-Cre is a transgenic mouse line targeting slow-twitch fatigue-resistant and fast-twitch fatigue-resistant motor neurons that innervate oxidative type I and type IIa muscle fibers. To ablate these neurons, VAChT-Cre mice were crossbred with NSE-DTA mice, leading to the expression of diphtheria toxin A after Cre-mediated excision. The resulting VAChT-Cre;NSE-DTA mice exhibited motor deficits, abnormal locomotion, muscular atrophy, and tremor, making them a useful model for studying motor neuron physiology and pathology.
View Article and Find Full Text PDFTranscriptome signatures of the medial prefrontal cortex underlying GABAergic control of resilience to chronic stress exposure.
Mol Psychiatry
November 2024
Department of Biology, The Pennsylvania State University, University Park, PA, 16802, USA.
Analyses of postmortem human brains and preclinical studies of rodents have identified somatostatin (SST)-positive, dendrite-targeting GABAergic interneurons as key elements that regulate the vulnerability to stress-related psychiatric disorders. Conversely, genetically induced disinhibition of SST neurons (induced by Cre-mediated deletion of the γ2 GABA receptor subunit gene selectively from SST neurons, SSTCre:γ2 mice) results in stress resilience. Similarly, chronic chemogenetic activation of SST neurons in the medial prefrontal cortex (mPFC) results in stress resilience but only in male and not in female mice.
View Article and Find Full Text PDFHigh-fat and high-carbohydrate diets increase bone fragility through TGF-β-dependent control of osteocyte function.
JCI Insight
July 2024
Department of Orthopaedic Surgery, University of California, San Francisco, San Francisco, California, USA.
Obesity can increase the risk of bone fragility, even when bone mass is intact. This fragility stems from poor bone quality, potentially caused by deficiencies in bone matrix material properties. However, cellular and molecular mechanisms leading to obesity-related bone fragility are not fully understood.
View Article and Find Full Text PDFPTEN acts as a crucial inflammatory checkpoint controlling TLR9/IL-6 axis in B cells.
iScience
July 2024
Immunology Research Center, National Health Research Institutes, Zhunan Town, Miaoli County 350401, Taiwan.
Phosphatase and tensin homolog (PTEN) is vital for B cell development, acting as a key negative regulator in the PI3K signaling pathway. We used CD23-cre to generate PTEN-conditional knockout mice (CD23-cKO) to examine the impact of PTEN mutation on peripheral B cells. Unlike mb1-cre-mediated PTEN deletion in early B cells, CD23-cKO mutants exhibited systemic inflammation with increased IL-6 production in mature B cells upon CpG stimulation.
View Article and Find Full Text PDFDevelopment of a thermostable Cre/lox-based gene disruption system and in vivo manipulations of the megaplasmid pTT27 in Thermus thermophilus HB27.
Plasmid
December 2024
Department of Applied Chemistry, National Defense Academy, Hashirimizu 1-10-20, Yokosuka, Kanagawa 239-8686, Japan.
We previously reported the development of a Cre/lox-based gene disruption system for multiple markerless gene disruption in Thermus thermophilus; however, it was a time-consuming method because it functioned at 50 °C, the minimum growth temperature of T. thermophilus HB27. In the present study, we improved this system by introducing random mutations into the cre-expressing plasmid, pSH-Cre.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!