APC/C-Fzr regulates cardiac and myoblast cell numbers, and plays a crucial role during myoblast fusion

Autor(en): Drechsler, Maik
Meyer, Heiko
Wilmes, Ariane C.
Paululat, Achim 
Stichwörter: ANAPHASE-PROMOTING COMPLEX; APC/C; APC/C-FZR/CDH1-DEPENDENT REGULATION; Cdh1; Cell Biology; Cell cycle; DORSAL VESSEL; DROSOPHILA; Dumbfounded; EMBRYONIC MUSCLE DEVELOPMENT; Fizzy related; GENE; LAME DUCK; Muscle; Myoblast fusion; PROTEIN; Rolling pebbles; SOMATIC MUSCULATURE; TRANSCRIPTION
Erscheinungsdatum: 2018
Herausgeber: COMPANY BIOLOGISTS LTD
Journal: JOURNAL OF CELL SCIENCE
Volumen: 131
Ausgabe: 14
Zusammenfassung: 
Somatic muscles are formed by the iterative fusion of myoblasts into muscle fibres. This process is driven by the recurrent recruitment of proteins to the cell membrane to induce F-actin nucleation at the fusion site. Although several proteins involved in myoblast fusion have been identified, knowledge about their subcellular regulation is rather elusive. We identified the anaphase-promoting complex (APC/C) adaptor Fizzy related (Fzr) as an essential regulator of heart and muscle development. We show that APC/C-Fzr regulates the fusion of myoblasts as well as the mitotic exit of pericardial cells, cardioblasts and myoblasts. Surprisingly, overproliferation is not causative for the observed fusion defects. Instead, fzr mutants exhibit smaller F-actin foci at the fusion site and display reduced membrane breakdown between adjacent myoblasts. We show that lack of APC/C-Fzr causes accumulation and mislocalisation of Rols and Duf, two proteins involved in the fusion process. Duf seems to serve as direct substrate of the APC/C-Fzr and its destruction depends on the presence of distinct degron sequences. These novel findings indicate that protein destruction and turnover constitute major events during myoblast fusion.
ISSN: 00219533
DOI: 10.1242/jcs.209155

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