CDC50A is required for aminophospholipid transport and cell fusion in mouse C2C12 myoblasts

Research output: Contribution to journal › Journal article › Research › peer-review

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CDC50A is required for aminophospholipid transport and cell fusion in mouse C2C12 myoblasts. / Grifell-Junyent, Marta; Baum, Julia F.; Valimets, Silja; Herrmann, Andreas; Paulusma, Coen C.; Lopez-Marques, Rosa L.; Pomorski, Thomas Gunther.

In: Journal of Cell Science, Vol. 135, No. 5, jcs258649, 2022.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Grifell-Junyent, M, Baum, JF, Valimets, S, Herrmann, A, Paulusma, CC, Lopez-Marques, RL & Pomorski, TG 2022, 'CDC50A is required for aminophospholipid transport and cell fusion in mouse C2C12 myoblasts', Journal of Cell Science, vol. 135, no. 5, jcs258649. https://doi.org/10.1242/jcs.258649

APA

Grifell-Junyent, M., Baum, J. F., Valimets, S., Herrmann, A., Paulusma, C. C., Lopez-Marques, R. L., & Pomorski, T. G. (2022). CDC50A is required for aminophospholipid transport and cell fusion in mouse C2C12 myoblasts. Journal of Cell Science, 135(5), [jcs258649]. https://doi.org/10.1242/jcs.258649

Vancouver

Grifell-Junyent M, Baum JF, Valimets S, Herrmann A, Paulusma CC, Lopez-Marques RL et al. CDC50A is required for aminophospholipid transport and cell fusion in mouse C2C12 myoblasts. Journal of Cell Science. 2022;135(5). jcs258649. https://doi.org/10.1242/jcs.258649

Author

Grifell-Junyent, Marta ; Baum, Julia F. ; Valimets, Silja ; Herrmann, Andreas ; Paulusma, Coen C. ; Lopez-Marques, Rosa L. ; Pomorski, Thomas Gunther. / CDC50A is required for aminophospholipid transport and cell fusion in mouse C2C12 myoblasts. In: Journal of Cell Science. 2022 ; Vol. 135, No. 5.

Bibtex

@article{bd3a882982b2439195fd6f32fcc94b0b,

title = "CDC50A is required for aminophospholipid transport and cell fusion in mouse C2C12 myoblasts",

abstract = "Myoblast fusion is essential for the formation of multinucleated muscle fibers and is promoted by transient changes in the plasma membrane lipid distribution. However, little is known about the lipid transporters regulating these dynamic changes. Here, we show that proliferating myoblasts exhibit an aminophospholipid flippase activity that is downregulated during differentiation. Deletion of the P4-ATPase flippase subunit CDC50A (also known as TMEM30A) results in loss of the aminophospholipid flippase activity and compromises actin remodeling, RAC1 GTPase membrane targeting and cell fusion. In contrast, deletion of the P4-ATPase ATP11A affects aminophospholipid uptake without having a strong impact on cell fusion. Our results demonstrate that myoblast fusion depends on CDC50A and may involve multiple CDC50A-dependent P4-ATPases that help to regulate actin remodeling.",

keywords = "Aminophospholipid translocase, Myogenesis, P4-ATPase, Phospholipid, Skeletal myoblasts",

author = "Marta Grifell-Junyent and Baum, {Julia F.} and Silja Valimets and Andreas Herrmann and Paulusma, {Coen C.} and Lopez-Marques, {Rosa L.} and Pomorski, {Thomas Gunther}",

year = "2022",

doi = "10.1242/jcs.258649",

language = "English",

volume = "135",

journal = "Journal of Cell Science",

issn = "0021-9533",

publisher = "The/Company of Biologists Ltd.",

number = "5",

}

RIS

TY - JOUR

T1 - CDC50A is required for aminophospholipid transport and cell fusion in mouse C2C12 myoblasts

AU - Grifell-Junyent, Marta

AU - Baum, Julia F.

AU - Valimets, Silja

AU - Herrmann, Andreas

AU - Paulusma, Coen C.

AU - Lopez-Marques, Rosa L.

AU - Pomorski, Thomas Gunther

PY - 2022

Y1 - 2022

N2 - Myoblast fusion is essential for the formation of multinucleated muscle fibers and is promoted by transient changes in the plasma membrane lipid distribution. However, little is known about the lipid transporters regulating these dynamic changes. Here, we show that proliferating myoblasts exhibit an aminophospholipid flippase activity that is downregulated during differentiation. Deletion of the P4-ATPase flippase subunit CDC50A (also known as TMEM30A) results in loss of the aminophospholipid flippase activity and compromises actin remodeling, RAC1 GTPase membrane targeting and cell fusion. In contrast, deletion of the P4-ATPase ATP11A affects aminophospholipid uptake without having a strong impact on cell fusion. Our results demonstrate that myoblast fusion depends on CDC50A and may involve multiple CDC50A-dependent P4-ATPases that help to regulate actin remodeling.

AB - Myoblast fusion is essential for the formation of multinucleated muscle fibers and is promoted by transient changes in the plasma membrane lipid distribution. However, little is known about the lipid transporters regulating these dynamic changes. Here, we show that proliferating myoblasts exhibit an aminophospholipid flippase activity that is downregulated during differentiation. Deletion of the P4-ATPase flippase subunit CDC50A (also known as TMEM30A) results in loss of the aminophospholipid flippase activity and compromises actin remodeling, RAC1 GTPase membrane targeting and cell fusion. In contrast, deletion of the P4-ATPase ATP11A affects aminophospholipid uptake without having a strong impact on cell fusion. Our results demonstrate that myoblast fusion depends on CDC50A and may involve multiple CDC50A-dependent P4-ATPases that help to regulate actin remodeling.

KW - Aminophospholipid translocase

KW - Myogenesis

KW - P4-ATPase

KW - Phospholipid

KW - Skeletal myoblasts

U2 - 10.1242/jcs.258649

DO - 10.1242/jcs.258649

M3 - Journal article

C2 - 34664668

AN - SCOPUS:85118305345

VL - 135

JO - Journal of Cell Science

JF - Journal of Cell Science

SN - 0021-9533

IS - 5

M1 - jcs258649

ER -

ID: 290601675