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Overlapping expression domains of bone morphogenetic protein family members potentially account for limited tissue
1Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.
Abstract:
BMP7 is expressed at diverse sites in the developing mouse embryo, including visceral endoderm, notochord, heart, eye, kidney, and bone. A null mutation in BMP7 results in defects largely confined to the developing kidney and eye. To examine whether other bone morphogenetic protein (BMP) family members potentially substitute for BMP7 in mutant embryos, thereby restricting the observed defects, we analyzed the expression patterns of BMP2 through BMP7 in wild-type and mutant tissues. In the central nervous system and heart, which develop normally in the absence of BMP7 signaling, expression domains of other BMP family members completely overlap with that of BMP7. The variable expressivity of the eye defect correlates with partially overlapping BMP4 and BMP7 expression domains during early eye induction. The loss of BMP7 signaling in the kidney results in apoptosis in the metanephric mesenchyme, a cell population that exclusively expresses BMP7. Thus, tissue defects observed in BMP7 deficient embryos are restricted to cell populations exclusively expressing BMP7. These data suggest that BMP family members can functionally substitute for BMP7 at sites where they colocalize in vivo.
Insights
Bone Morphogenetic Protein 7 (BMP7) loss causes defects in mouse kidneys and eyes. Other BMPs can substitute for BMP7 where their expression overlaps, limiting observed defects.
Area of Science:
- Developmental Biology
- Molecular Biology
- Genetics
Background:
- Bone Morphogenetic Protein 7 (BMP7) is crucial for embryonic development.
- BMP7 null mutations in mice primarily affect kidney and eye development.
- The potential for functional redundancy among Bone Morphogenetic Protein (BMP) family members remains to be fully elucidated.
Purpose of the Study:
- To investigate if other BMP family members can compensate for the loss of BMP7 in mutant mouse embryos.
- To correlate BMP expression patterns with observed developmental defects in BMP7-deficient mice.
- To understand the functional specificity of BMP7 during embryonic development.
Main Methods:
- Comparative analysis of BMP2-BMP7 expression patterns in wild-type and BMP7-mutant mouse embryos.
- Examination of tissue-specific expression domains of various BMPs.
- Assessment of apoptosis in developing kidney tissues of BMP7-deficient embryos.
Main Results:
- In tissues developing normally without BMP7 signaling (CNS, heart), other BMPs showed overlapping expression with BMP7.
- Variable eye defects in BMP7 mutants correlated with partial overlap between BMP4 and BMP7 expression.
- Loss of BMP7 in the kidney led to apoptosis specifically in the BMP7-expressing metanephric mesenchyme.
Conclusions:
- BMP7 deficiency leads to defects primarily in tissues exclusively expressing BMP7.
- Other BMP family members can functionally substitute for BMP7 where their expression domains overlap in vivo.
- BMP family member colocalization is critical for functional redundancy in embryonic development.