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BMP7 functions predominantly as a heterodimer with BMP2 or BMP4 during mammalian embryogenesis

Hyung-Seok Kim, Judith Neugebauer, Autumn McKnite, Anup Tilak, View ORCID ProfileJan L. Christian
doi: https://doi.org/10.1101/686758
Hyung-Seok Kim
1Department of Neurobiology and Anatomy and Internal Medicine, Division of Hematology and Hematologic Malignancies, University of Utah, School of Medicine, Salt Lake City, UT 94132 USA
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Judith Neugebauer
1Department of Neurobiology and Anatomy and Internal Medicine, Division of Hematology and Hematologic Malignancies, University of Utah, School of Medicine, Salt Lake City, UT 94132 USA
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Autumn McKnite
1Department of Neurobiology and Anatomy and Internal Medicine, Division of Hematology and Hematologic Malignancies, University of Utah, School of Medicine, Salt Lake City, UT 94132 USA
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Anup Tilak
2Department of Cell and Developmental Biology, Oregon Health and Sciences University, School of Medicine, Portland, OR 97239-3098 USA
£Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN 55455
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Jan L. Christian
1Department of Neurobiology and Anatomy and Internal Medicine, Division of Hematology and Hematologic Malignancies, University of Utah, School of Medicine, Salt Lake City, UT 94132 USA
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  • ORCID record for Jan L. Christian
  • For correspondence: jan.christian@neuro.utah.edu
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Abstract

BMP7/BMP2 or BMP7/BMP4 heterodimers are more active than homodimers in vitro, but it is not known whether these heterodimers signal in vivo. To test this, we generated knock in mice carrying a mutation (Bmp7R-GFlag) that prevents proteolytic activation of the dimerized BMP7 precursor protein. This mutation eliminates the function of BMP7 homodimers and all other BMPs that normally heterodimerize with BMP7. While Bmp7 null homozygotes are live born, Bmp7R-GFlag homozygotes are embryonic lethal and have broadly reduced BMP activity. Furthermore, compound heterozygotes carrying the Bmp7R-G allele together with a null allele of Bmp2 or Bmp4 die during embryogenesis with defects in ventral body wall closure and/or the heart. Co-immunoprecipitation assays confirm that endogenous BMP4/7 heterodimers exist. Thus, BMP7 functions predominantly as a heterodimer with BMP2 or BMP4 during mammalian development, which may explain why mutations in either Bmp4 or Bmp7 lead to a similar spectrum of congenital defects in humans.

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Posted June 28, 2019.
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BMP7 functions predominantly as a heterodimer with BMP2 or BMP4 during mammalian embryogenesis
Hyung-Seok Kim, Judith Neugebauer, Autumn McKnite, Anup Tilak, Jan L. Christian
bioRxiv 686758; doi: https://doi.org/10.1101/686758
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BMP7 functions predominantly as a heterodimer with BMP2 or BMP4 during mammalian embryogenesis
Hyung-Seok Kim, Judith Neugebauer, Autumn McKnite, Anup Tilak, Jan L. Christian
bioRxiv 686758; doi: https://doi.org/10.1101/686758

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