Actomyosin-mediated tension orchestrates uncoupled respiration in adipose tissues
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA432141 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6652620.fastq.gz | Fastqsanger.gz | |||
| SRR6652621.fastq.gz | Fastqsanger.gz | |||
| SRR6652622.fastq.gz | Fastqsanger.gz | |||
| SRR6652623.fastq.gz | Fastqsanger.gz | |||
| SRR6652624.fastq.gz | Fastqsanger.gz |
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Project description:The activation of brown/beige adipose tissue (BAT) metabolism and the induction of uncoupling protein-1 (UCP1) expression are essential for BAT-based strategies to improve metabolic homeostasis. Adrenergic signaling is viewed as a key regulator of thermogenesis and UCP1-expression in BAT, while also operating as a potent contractile stimulator in muscle. The muscle-like gene expression patterns of UCP1+ adipocytes have previously been utilized as tissue specific markers, but have not been attributed with any functional role. Here, we demonstrate that BAT utilizes actomyosin machinery to generate tensional responses following adrenergic stimulation, similar to muscle tissues. We show that activation of actomyosin mechanics are critical for the acute induction of oxidative metabolism and uncoupled respiration in UCP1+ adipocytes. Additionally, actomyosin-mediated elasticity regulates mechanosensitive transcriptional co-activators, YAP/TAZ, that facilitate the thermogenic capacity of adipocytes. These unappreciated signaling and mechanical mechanisms may inform future strategies to promote the expansion and activation of brown/beige adipocytes.
2018-03-01 | GSE109829 | GEO
Project description:The activation of brown/beige adipose tissue (BAT) metabolism and the induction of uncoupling protein 1 (UCP1) expression are essential for BAT-based strategies to improve metabolic homeostasis. Here, we demonstrate that BAT utilizes actomyosin machinery to generate tensional responses following adrenergic stimulation, similar to muscle tissues. The activation of actomyosin mechanics is critical for the acute induction of oxidative metabolism and uncoupled respiration in UCP1+ adipocytes. Moreover, we show that actomyosin-mediated elasticity regulates the thermogenic capacity of adipocytes via the mechanosensitive transcriptional co-activators YAP and TAZ, which are indispensable for normal BAT function. These biomechanical signaling mechanisms may inform future strategies to promote the expansion and activation of brown/beige adipocytes.
| S-EPMC5897043 | biostudies-literature
Project description:For placental mammals, the transition from the in utero maternal environment to postnatal life requires the activation of thermogenesis to maintain their core temperature. This is primarily accomplished by induction of uncoupling protein 1 (UCP1) in brown and beige adipocytes, the principal sites for uncoupled respiration. Despite its importance, how placental mammals license their thermogenic adipocytes to participate in postnatal uncoupled respiration is not known. Here, we provide evidence that the 'alarmin' IL-33, a nuclear cytokine that activates type 2 immune responses, licenses brown and beige adipocytes for uncoupled respiration. We find that, in absence of IL-33 or ST2, beige and brown adipocytes develop normally but fail to express an appropriately spliced form of Ucp1 mRNA, resulting in absence of UCP1 protein, and impairment in uncoupled respiration and thermoregulation. Together, these data suggest that IL-33 and ST2 function as a developmental switch to license thermogenesis during the perinatal period.
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Project description:It has been a long-standing challenge to maintain the functions of hepatocytes in vitro. In the present study, we found that mechanical tension-induced yes-associated protein (Yap) activation triggered hepatocyte dedifferentiation. Alleviation of mechanical tension by confinement of cell spreading was sufficient to inhibit hepatocyte dedifferentiation. Based on this finding, we identified a small molecular cocktail LBDXL through reiterative chemical screening that could maintain hepatocyte functions over the long term and in vivo repopulation capacity by targeting actin polymerization and actomyosin contraction.
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Project description:Actomyosin contractility regulates cell morphology and movement. The objective of this study was to identify whether actomyosin contractility regulates gene expression in tumour cells and whether such genes are involved in cell morphology and movement. Gene expression analysis was carried out on highly contractile melanoma cell line A375M2 plated on a deformable collagen matrix under conditions where actomyosin contractility could be altered following treatment with blebbistatin, a direct inhibitor of myosin II, or Rho-kinase inhibitors Y27632 or H1152 that interfere with signalling to myosin II. 18 samples (6 x 3 biological replicates). Cells were plated on rigid or deformable matrices. Rounded cells (A375M2 melanoma cells) plated on deformable matrices were left untreated or treated with Rho-kinase inhibitors Y27632, H1152 or blebbistatin an inhibitor of mysoin II.
2010-08-24 | E-GEOD-23764 | biostudies-arrayexpress
Project description:Actomyosin contractility regulates cell morphology and movement. The objective of this study was to identify whether actomyosin contractility regulates gene expression in tumour cells and whether such genes are involved in cell morphology and movement. Gene expression analysis was carried out on highly contractile melanoma cell line A375M2 plated on a deformable collagen matrix under conditions where actomyosin contractility could be altered following treatment with blebbistatin, a direct inhibitor of myosin II, or Rho-kinase inhibitors Y27632 or H1152 that interfere with signalling to myosin II.
2010-08-24 | GSE23764 | GEO
Project description:During morphogenesis, molecular mechanisms that orchestrate biomechanical dynamics across cells remain unclear. Here, we show a role of guidance receptor Plexin-B2 in organizing actomyosin network and adhesion complexes during multicellular development of human embryonic stem cells and neuroprogenitor cells. Plexin-B2 manipulations affect actomyosin contractility, leading to changes in cell stiffness and cytoskeletal tension, as well as cell-cell and cell-matrix adhesion. We have delineated the functional domains of Plexin-B2, RAP1/2 effectors, and the signaling association with ERK1/2, calcium activation, and YAP mechanosensor, thus providing a mechanistic link between Plexin-B2-mediated cytoskeletal tension and stem cell physiology. Plexin-B2-deficient stem cells exhibit premature lineage commitment, and a balanced level of Plexin-B2 activity is critical for maintaining cytoarchitectural integrity of the developing neuroepithelium, as modeled in cerebral organoids. Our studies thus establish a significant function of Plexin-B2 in orchestrating cytoskeletal tension and cell-cell/cell-matrix adhesion, therefore solidifying the importance of collective cell mechanics in governing stem cell physiology and tissue morphogenesis.
| S-EPMC8517024 | biostudies-literature
Project description:One of the most common cell shape changes driving morphogenesis in diverse animals is the constriction of the apical surface. Apical constriction depends on contraction of an actomyosin network in the apical cell cortex, but such actomyosin networks have been shown to undergo continual, conveyor belt-like contractions even before the shrinking of an apical surface begins. This finding suggests that apical constriction is not necessarily triggered by the contraction of actomyosin networks, but rather by unidentified, temporally-regulated mechanical linking of actomyosin to the cell junctions. Here, we used C. elegans gastrulation as a model to identify proteins that contribute to such linkage. We found that α-catenin and β-catenin initially failed to move centripetally with contracting cortical actomyosin networks, suggesting that linkage is regulated between cadherin-catenin complexes and actomyosin. We used a proteomic approach to identify AFD-1/afadin and transcriptomics to identify ZYX-1/zyxin as contributors to C. elegans gastrulation. We found that a zyxin family of LIM domain proteins have transcripts that become enriched in multiple cells just before they undergo apical constriction. Using a new, semi-automated image analysis tool, we found that AFD-1/afadin and ZYX-1/zyxin both contribute to cell-cell junctions’ centripetal movement along contracting actomyosin networks. These results identify two key proteins as important for actomyosin networks to effectively pull cell-cell junctions inward during apical constriction. The transcriptional upregulation of zyxin/ZYX-1 in specific cells points to one way that developmental patterning spatiotemporally regulates cell biological mechanisms in vivo. Because afadin- and zyxin-family proteins contribute to membrane-cytoskeleton linkage in other systems, we anticipate that their roles in regulating apical constriction in this manner may be conserved.
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Project description:We recently reported that the loss of the microRNA cluster miR-379-410 leads to hypersocial behavior and anxiety in mice. With this study, we show that ablating miR-379-410 in excitatory neurons of the postnatal mouse hippocampus recapitulates hypersociability, but not anxiety. At the cellular level, miR-379-410 loss in excitatory neurons leads to increased excitatory synaptic transmission and upregulation of an actomyosin gene network. Re-expression of three cluster miRNAs, as well as pharmacological inhibition of the actomyosin activator ROCK, was sufficient to reinstate normal sociability in miR-379-410 knockout mice. Our results unveil a novel microRNA-actomyosin pathway involved in the control of sociability.
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Project description:Actomyosin contractility represents an ancient feature of eukaryotic cells participating in many developmental and homeostasis events, including tissue morphogenesis, muscle contraction, and cell migration, with dysregulation implicated in various pathological conditions, such as cancer. At the molecular level, actomyosin comprises actin bundles and myosin motor proteins that are sensitive to posttranslational modifications like phosphorylation. While the molecular components of actomyosin and its regulation are well understood, the coordination of contractility by extracellular and intracellular signals, particularly from cellular signaling pathways, remains incompletely elucidated. This study focuses on planar cell polarity (PCP) signaling, previously associated with actomyosin contractility during vertebrate neurulation. Contrary to previous studies, our investigation reveals that main cytoplasmic PCP proteins, Prickle and Dishevelled, interact directly with key actomyosin components such as myosin light chain (MLC), leading to its phosphorylation and localized activation. Through relevant in vitro and in vivo models, we demonstrate that these PCP proteins function not merely passively and indirectly as previously reported, but that they actively control actomyosin contractility by acting as scaffold proteins, orchestrating the necessary machinery for contractility. These findings unveil a direct link of PCP signaling in crucial actomyosin contractility processes through MLC that are relevant to vertebrate neurulation and potentially beyond.
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