4.5 Article

PIP3 depletion rescues myoblast fusion defects in human rhabdomyosarcoma cells

Journal

JOURNAL OF CELL SCIENCE
Volume 133, Issue 8, Pages -

Publisher

COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.240325

Keywords

Phosphatidylinositol-(3,4,5)-trisphosphate; Myoblast fusion; Rhabdomyosarcoma; Myogenesis; Bleb; PTEN

Categories

Funding

  1. Ministry of Science and Technology, Taiwan [MOST 108-2320-B-007-005-MY3, 107-2628-B-007-001, 108-2636-B-007-003, 109-2636-B-007-003, 108-2638-B-010-001-MY2]
  2. National Health Research Institutes, Taiwan [NHRI-EX109-10813NI]

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Myoblast fusion is required for myotube formation during myogenesis, and defects in myoblast differentiation and fusion have been implicated in a number of diseases, including human rhabdomyosarcoma. Although transcriptional regulation of the myogenic program has been studied extensively, the mechanisms controlling myoblast fusion remain largely unknown. This study identified and characterized the dynamics of a distinct class of blebs, termed bubbling blebs, which are smaller than those that participate in migration. The formation of these bubbling blebs occurred during differentiation and decreased alongside a decline in phosphatidylinositol-(3,4,5)-trisphosphate (PIP3) at the plasma membrane before myoblast fusion. In a human rhabdomyosarcoma-derived (RD) cell line that exhibits strong blebbing dynamics and myoblast fusion defects, PIP3 was constitutively abundant on the membrane during myogenesis. Targeting phosphatase and tensin homolog (PTEN) to the plasma membrane reduced PIP3 levels, inhibited bubbling blebs and rescued myoblast fusion defects in RD cells. These findings highlight the differential distribution and crucial role of PIP3 during myoblast fusion and reveal a novel mechanism underlying myogenesis defects in human rhabdomyosarcoma.

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