Redundancy of myostatin and growth/differentiation factor 11 function.

Full Abstract

BACKGROUND: Myostatin (Mstn) and growth/differentiation factor 11 (Gdf11) are highly related transforming growth factor beta (TGFbeta) family members that play important roles in regulating embryonic development and adult tissue homeostasis. Despite their high degree of sequence identity, targeted mutations in these genes result in non-overlapping phenotypes affecting distinct biological processes. Loss of Mstn in mice causes a doubling of skeletal muscle mass while loss of Gdf11 in mice causes dramatic anterior homeotic transformations of the axial skeleton, kidney agenesis, and an increase in progenitor cell number in several tissues. In order to investigate the possible functional redundancy of myostatin and Gdf11, we analyzed the effect of eliminating the functions of both of these signaling molecules. RESULTS: We show that Mstn-/- Gdf11-/- mice have more extensive homeotic transformations of the axial skeleton than Gdf11-/- mice in addition to skeletal defects not seen in single mutants such as extra forelimbs. We also show that deletion of Gdf11 specifically in skeletal muscle in either Mstn+/+ or Mstn-/- mice does not affect muscle size, fiber number, or fiber type. CONCLUSION: These results provide evidence that myostatin and Gdf11 have redundant functions in regulating skeletal patterning in mice but most likely not in regulating muscle size.

Author information

Author/s: McPherron, Alexandra C (AC); Huynh, Thanh V (TV); Lee, Se-Jin (SJ);

Affiliation: Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892, USA. mcpherrona(-atsign-)niddk.nih.gov

Grants: R01HD35887 (Agency:NICHD NIH HHS) ; U54AR052646 (Agency:NIAMS NIH HHS)

Journal and publication information

Publication Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural

Journal: BMC developmental biology (BMC Dev Biol), published in England. (Language: eng)

Reference: 2009-; vol 9 (issue ) : pp 24

Dates: Created 2009/04/08; Completed 2009/05/22;

PMID: 19298661, status: MEDLINE (last retrieved date: 5/22/2009)

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MeSH Headings (categories) shown below.

Animals
Bone Development
Bone Morphogenetic Proteins - genetics; metabolism
Female
Gene Expression Regulation, Developmental
Growth Differentiation Factors - genetics; metabolism

Note: Bold headings indicate primary MeSH headings or qualifiers.

Associated Chemicals: Bone Morphogenetic Proteins (0) ; Gdf11 protein, mouse (0) ; Growth Differentiation Factors (0) ; Mstn protein, mouse (0) ; Myostatin (0)

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