Response: Contributions of the Myf5-independent lineage to myogenesis

Malay Haldar; Goutam Karan; Shuichi Watanabe; Stefan Guenther; Thomas Braun; Mario R Capecchi

doi:10.1016/j.devcel.2014.11.010

Response: Contributions of the Myf5-independent lineage to myogenesis

Dev Cell. 2014 Dec 8;31(5):539-41. doi: 10.1016/j.devcel.2014.11.010.

Authors

Malay Haldar¹, Goutam Karan², Shuichi Watanabe³, Stefan Guenther³, Thomas Braun³, Mario R Capecchi⁴

Affiliations

¹ Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
² MiRx Pharmaceuticals and Invenio Therapeutics, Lexington, KY 40502, USA.
³ Max-Planck-Institute for Heart and Lung Research, Department of Cardiac Development and Remodeling, Parkstrasse 1, D-61231 Bad Nauheim, Hessen, Germany.
⁴ Howard Hughes Medical Institute, University of Utah, Salt Lake City, UT 84112, USA; Department of Human Genetics, University of Utah, Salt Lake City, UT 84112, USA. Electronic address: mario.capecchi@genetics.utah.edu.

Abstract

In this issue, Comai et al. present evidence that previous support for Myf5-independent myogenic cell lineages was confounded by inefficiencies in lineage marking and ablation. Here, Haldar et al. discuss other possible explanations for the inconsistencies between different data sets and reiterate their views on Myf5-independent myogenesis.

Publication types

Letter
Comment

MeSH terms

Animals
Cell Lineage*
DNA-Binding Proteins / metabolism*
Muscle Proteins / metabolism*
Muscle, Skeletal / cytology*
Myogenic Regulatory Factor 5 / metabolism*

Substances

DNA-Binding Proteins
Muscle Proteins
Myf5 protein, mouse
Myogenic Regulatory Factor 5

Grants and funding

R01 GM021168/GM/NIGMS NIH HHS/United States