Functional analysis of activins during mammalian development

ACTIVINS are dimeric (βAβA; βBβB; βAβB) members of the transforming growth factor-β superfamily 1 . They are widely expressed during murine development 1–6 , are highly conserved during vertebrate evolution 1,7–11 , and may be involved in mesoderm induction and neurulation in Xenopus laevis and Oryz...

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Bibliographic Details
Published in:Nature (London) 1995-03, Vol.374 (6520), p.354-357
Main Authors: Matzuk, Martin M, Kumar, T. Rajendra, Vassalli, Anne, Bickenbach, Jackie R, Roop, Dennis R, Jaenisch, Rudolf, Bradley, Allan
Format: Article
Language:English
Subjects:
Activins
Animals
Biological and medical sciences
Cell Line
Cellular biology
Embryology: invertebrates and vertebrates. Teratology
Embryonic and Fetal Development - physiology
Embryonic growth stage
Experimental organogenesis
Fundamental and applied biological sciences. Psychology
Genetics
Growth Substances - physiology
Humanities and Social Sciences
Inhibins - genetics
Inhibins - physiology
letter
Mammals
Mice
Mice, Inbred C57BL
multidisciplinary
Mutation
Organogenesis. Physiological fonctions
Palate - abnormalities
Palate - embryology
Rodents
Science
Science (multidisciplinary)
Skull - abnormalities
Skull - embryology
Transforming Growth Factor beta - physiology
Vertebrates
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Summary:ACTIVINS are dimeric (βAβA; βBβB; βAβB) members of the transforming growth factor-β superfamily 1 . They are widely expressed during murine development 1–6 , are highly conserved during vertebrate evolution 1,7–11 , and may be involved in mesoderm induction and neurulation in Xenopus laevis and Oryzias latipes 10–17 . To investigate the function of mammalian activins in vivo , we generated mice with mutations either in activin-βA or in both activin-βA and activin-βB. Activin-βA-deficient mice develop to term but die within 24 h of birth. They lack whiskers and lower incisors and have defects in their secondary palates, including cleft palate, demonstrating that activin-βA must have a role during craniofacial development. Mice lacking both activin subunits show the defects of both individual mutants but no additional defects, indicating that there is no functional redundancy between these proteins during embryogenesis. In contrast to observations in lower vertebrates 10–17 , zygotic expression of activins is not essential for mesoderm formation in mice.
ISSN:0028-0836
1476-4687
DOI:10.1038/374354a0