GAS2L3: Coordinator of cardiomyocyte cytokinesis?

Gründl, Marco; Engel, Felix B.; Gaubatz, Stefan

doi:10.1080/15384101.2017.1372546

Cited by 3 publications

(4 citation statements)

References 7 publications

(8 reference statements)

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“…The proliferation arrest of CMs is accompanied by binucleation through incomplete cytokinesis. Whether this protein might be involved in the physiological propensity of CMs to undergo bi‐ and multinucleation after birth remains a matter for interesting future investigation .…”

Section: Dynamics Of the Centrosome During Cardiomyocyte Mitosis And mentioning

confidence: 99%

Cardiac regeneration and remodelling of the cardiomyocyte cytoarchitecture

2019

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Adult mammals are unable to regenerate their hearts after cardiac injury, largely due to the incapacity of cardiomyocytes (CMs) to undergo cell division. However, mammalian embryonic and fetal CMs, similar to CMs from fish and amphibians during their entire life, exhibit robust replicative activity, which stops abruptly after birth and never significantly resumes. Converging evidence indicates that formation of the highly ordered and stable cytoarchitecture of mammalian mature CMs is coupled with loss of their proliferative potential. Here, we review the available information on the role of the cardiac cytoskeleton and sarcomere in the regulation of CM proliferation. The actin cytoskeleton, the intercalated disc, the microtubular network and the dystrophin-glycoprotein complex each sense mechanical cues from the surrounding environment. Furthermore, they participate in the regulation of CM proliferation by impinging on the yes-associated protein/transcriptional co-activator with PDZ-binding motif, b-catenin and myocardin-related transcription factor transcriptional co-activators. Mastering the molecular mechanisms regulating CM proliferation would permit the development of innovative strategies to stimulate cardiac regeneration in adult individuals, a hitherto unachieved yet fundamental therapeutic goal.

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Section: Dynamics Of the Centrosome During Cardiomyocyte Mitosis And mentioning

confidence: 99%

Cardiac regeneration and remodelling of the cardiomyocyte cytoarchitecture

2019

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“…16 The normal expression of GAS2L3 is important for abscission in the last step of HeLa cell cytokinesis, 16,20,21,38 and for cardiomyocyte cytokinesis in mice. 29,39 The cell-free systems from both, Xenopus laevis egg and human HEK293 cells, were utilized by Pe'er, T., et al In 2013, a study revealed that GAS2L3 protein serves as a substrate of anaphase promoting complex/cyclosome (APC/C) and can be degraded in a Cadherin 1 (CDH1)-mediated ubiquitin proteasome pathway. 20 The destruction box (D-box) with ' 610 R/T/P/L 613 ' motif of GAS2L3 was thought to be essential for GAS2L3 degradation in G1 extracts.…”

Section: Cell Cyclementioning

confidence: 99%

“…On the contrary, the expression level gradually increases when the cell re‐enters the cell cycle and reaches a peak in the G2/M phase 16 . The normal expression of GAS2L3 is important for abscission in the last step of HeLa cell cytokinesis, 16,20,21,38 and for cardiomyocyte cytokinesis in mice 29,39 . The cell‐free systems from both, Xenopus laevis egg and human HEK293 cells, were utilized by Pe'er, T., et al In 2013, a study revealed that GAS2L3 protein serves as a substrate of anaphase promoting complex/cyclosome (APC/C) and can be degraded in a Cadherin 1 (CDH1)‐mediated ubiquitin proteasome pathway 20 .…”

Section: Biological Functionmentioning

confidence: 99%

Growth arrest–specific 2 protein family: Structure and function

et al. 2020

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It is widely believed that the cytoskeletal system of the mammalian cell, a type of protein fibre grid system, contains microtubules, actin and intermediate filaments, and contributes to the morphological integrity and cell polarity. 1,2 In the past decade, scientists have performed extensive studies on the biological structures and behavioural modulation mechanisms of cytoskeletal components in various cellular environments. Emerging evidence supports the finding that the dynamic coordinated action between microtubules and

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“…G2L3 knockout mice die early after birth because of cytokinesis defects 14 . Depletion of G2L3 resulted in defects in chromosome separation 15,16 , and overexpression of G2L3 specifically interferes with cell abscission at the final stage of cell division 17 . In addition to having a role in regulating cell motility 12 , G2L1 has also been reported to regulate centrosome splitting by mediating actin-microtubule crosstalk 1 .…”

Section: Introductionmentioning

confidence: 99%

GAS2-like 1 coordinates cell division through its association with end-binding proteins

Nazgiewicz

Atherton

Ballestrem

2019

Sci Rep

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Cell division involves the tightly coordinated rearrangement of actin and microtubules (MTs). We have previously shown that a member of the family of growth arrest-specific 2-like proteins, GAS2-like 1 (G2L1) regulates actin-MT crosstalk through its associations with plus-end microtubule tip-binding (EB) proteins. Here we show that G2L1 is involved in the regulation of cell division. We show that the depletion of G2L1 results in a reduction in the number of cells undergoing cell division and a significant proportion of those cells that do divide are either multinucleated, display deformed nuclei, or undergo cell division at a much slower rate. Exogenous expression of G2L1 mutants revealed that the association of G2L1 with EB1 is critical for regulated cell division and blocking this interaction inhibits cell division as observed in cells lacking G2L1. Taken together, our data suggest that G2L1 controls the precise regulation and successful progression of cell division through its binding to EB-proteins.

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GAS2L3: Coordinator of cardiomyocyte cytokinesis?

Cited by 3 publications

References 7 publications

Cardiac regeneration and remodelling of the cardiomyocyte cytoarchitecture

Cardiac regeneration and remodelling of the cardiomyocyte cytoarchitecture

Growth arrest–specific 2 protein family: Structure and function

GAS2-like 1 coordinates cell division through its association with end-binding proteins

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