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Ubiquitin-dependent remodeling of the actin cytoskeleton drives cell fusion

ABSTRACT: Ubiquitin-dependent remodeling of the actin cytoskeleton drives cell fusion

PROVIDER: PRJNA679071 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13076473_1.fastq.gz	Fastqsanger.gz
	SRR13076473_2.fastq.gz	Fastqsanger.gz
	SRR13076474_1.fastq.gz	Fastqsanger.gz
	SRR13076474_2.fastq.gz	Fastqsanger.gz
	SRR13076475_1.fastq.gz	Fastqsanger.gz

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Ubiquitin-dependent remodeling of the actin cytoskeleton drives cell fusion

Project description:Cell-cell fusion is a frequent and essential event during development, and its dysregulation causes diseases ranging from infertility to muscle weakness. Fusing cells repeatedly need to remodel their plasma membrane by orchestrated formation and disassembly of cortical actin filaments, but how the dynamic reorganization of the actin cytoskeleton control is still poorly understood. Here, we identified a ubiquitin- dependent toggle switch that establishes reversible actin bundling during mammalian cell fusion. We found that EPS8-IRSp53 complexes stabilize cortical actin bundles at sites of cell contact, which in part pushes cells towards each other. Conversely, EPS8 monoubiquitylation by CUL3KCTD10 displaces EPS8-IRSp53 from membranes and counteracts actin bundling, a dual activity that allows apposed cells to progress with fusion. We conclude that cytoskeletal rearrangements during development are precisely controlled by ubiquitylation, raising the possibility to modulate the efficiency of cell-cell fusion for therapeutic benefit.

2020-12-22 | GSE161681 | GEO

PTBP1 mediates Sertoli cell actin cytoskeleton organization through regulating alternative splicing of actin regulators

Project description:Spermatogenesis is a biological process within the testis that produces haploid spermatozoa for the continuity of species. Sertoli cells are somatic cells in the seminiferous epithelium that orchestrate spermatogenesis. Cyclic reorganization of Sertoli cell actin cytoskeleton is vital for spermatogenesis but the underlying mechanism remains largely unclear. Here we report that RNA-binding protein PTBP1 controls Sertoli cell actin cytoskeleton reorganization by programming alternative splicing of actin cytoskeleton regulators. This splicing control enables ectoplasmic specializations, the actin-based adhesion junctions, to maintain the blood-testis barrier and support spermatid transport and transformation. Of particular, we show that PTBP1 promotes actin bundle formation by repressing the inclusion of exon 14 of Tnik, a kinase present at the ectoplasmic specialization. Our results thus reveal a novel mechanism wherein Sertoli cell actin cytoskeleton dynamics is controlled post-transcriptionally by utilizing functionally distinct isoforms of actin regulatory proteins and PTBP1 is a key player in generating such isoforms.

2024-07-31 | GSE267924 | GEO

Methylation of HBP1 by PRMT1 inhibits its tumor-suppressive function through regulating 2 GSN-mediated actin cytoskeleton remodeling

Project description:HBP1 is a sequence-specific transcription factor which acts as a tumor inhibitor. HBP1 exerts tumor-suppressive function through regulating the expression of many genes during cell metabolism and cell cycle process. Posttranslational modification of HBP1 is crucial for its function. In this study, we found that HBP1 was methylated at R378 by PRMT1, which decreased 16 HBP1 protein stability by promoting its ubiquitination and proteasome-mediated degradation. PRMT1-mediated methylation of HBP1 could alleviate the repressive effects of HBP1 on tumor metastasis and growth through regulation of GSN expression. GSN was identified as a novel target gene of HBP1. Methylation of HBP1 promoted actin cytoskeleton remodeling and tumor progression by downregulating GSN levels. The methylated HBP1-GSN axis was also associated with the clinical outcomes of cancer patients. Targeting methylated HBP1-GSN axis may provide a therapeutic strategy for cancer. Significance: This investigation elucidated the mechanism of how methylation of HBP1 at R378 inhibits its tumor-suppressive function and promotes actin cytoskeleton remodeling, thus providing the strategy for targeting HBP1 during cancer treatment.

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Actin Cytoskeleton Integrates Auxin and Brassinosteroid Signaling in Plants.

Project description:We describe a new mutant allele of the ACTIN2 gene with enhanced actin dynamics, displaying a broad array of twisting and bending phenotypes that resemble BR-treated plants. Moreover, auxin transcriptional regulation is enhanced on the mutant background, supporting the idea that shaping actin filaments is sufficient to modulate BR-mediated auxin responsiveness. The actin cytoskeleton thus functions as a scaffold for integration of auxin and BR signaling pathways.

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PTBP1 mediates Sertoli cell actin cytoskeleton organization through regulating alternative splicing of actin regulators

Project description:PTBP1 mediates Sertoli cell actin cytoskeleton organization through regulating alternative splicing of actin regulators

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KLF5 regulates actin remodeling to enhance the metastasis of nasopharyngeal carcinoma [RNA-seq]

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Project description:Methylation of HBP1 by PRMT1 inhibits its tumor-suppressive function through regulating 2 GSN-mediated actin cytoskeleton remodeling

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Large-scale genetic screens identify BET-1 as a cytoskeleton regulator promoting actin health and lifespan

Project description:The actin cytoskeleton is a three-dimensional scaffold of proteins that is a regulatory, energy-consuming material with dynamic properties shaping the structure and function of the cell. The proper function of actin is required for many cellular pathways, including cell division, autophagy, chaperone function, endocytosis, and exocytosis (1–5). The breakdown of these cellular processes manifests during aging and exposure to stress, which is in part due to the breakdown of the actin cytoskeleton (5–9). However, the regulatory mechanisms involved in preservation of cytoskeletal form and function are not well understood. Here, we performed a multi-pronged, cross-organismal screen combining a whole-genome CRISPR-Cas9 screen in human fibroblasts with in vivo C. elegans synthetic lethality screening. We identified the bromodomain protein, BET-1, as a key regulator promoting actin health and longevity. Interestingly, overexpression of bet-1 preserves actin health at late age and promotes lifespan and healthspan in C. elegans. These beneficial effects are through preservation of actin, downstream of the function of BET-1 as a transcriptional regulator. Together, our discovery attributes assigns a key role of BET-1 in cytoskeletal health, highlighting regulatory cellular networks promoting cytoskeletal homeostasis.

2023-06-01 | E-MTAB-12289 | biostudies-arrayexpress

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