What question did this study set out to answer?

To determine the in vivo physiological necessity of the calcitonin receptor-like receptor (CLR) and establish whether it mediates adrenomedullin signaling during embryonic development.

March 14, 2006Molecular and Cellular BiologyOpen Access

Hydrops Fetalis, Cardiovascular Defects, and Embryonic Lethality in Mice Lacking the Calcitonin Receptor-Like Receptor Gene

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Authors

RDRyan T. DackorUniversity of North Carolina at Chapel Hill KFKimberly L. Fritz-SixUniversity of North Carolina at Chapel Hill WDWilliam P. DunworthUniversity of North Carolina at Chapel Hill

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Implication

Knockout study demonstrates embryonic lethality and severe cardiovascular defects in Calcrl-deficient mice, indicating that CLR is an essential adrenomedullin receptor in vivo.

Key Points

To determine the in vivo physiological necessity of the calcitonin receptor-like receptor (CLR) and establish whether it mediates adrenomedullin signaling during embryonic development.
Generated a targeted gene-knockout mouse model lacking the Calcrl allele.
Performed timed matings to assess survival timing, gross embryological anatomy, and cardiovascular structure.
Conducted in vivo cellular proliferation and apoptosis assays in the hearts and vasculature of Calcrl-/- and AM-/- embryos.
Heterozygous Calcrl+/- mice survived to adulthood normally, whereas homozygous Calcrl-/- embryos suffered 100% embryonic lethality between embryonic day 13.5 (E13.5) and E14.5.
Calcrl-/- embryos exhibited severe hydrops fetalis, thin vascular smooth muscle walls, and small, disorganized hearts phenocopying AM-/- embryos.
In vivo assays of apoptosis and cellular proliferation confirmed that CLR functions as the primary mediator of adrenomedullin-dependent cardiovascular development.

Cite This Study

Dackor et al. (2006) studied this question.

synapsesocial.com/papers/6a76b4d16783c23f50254792 https://doi.org/10.1128/mcb.26.7.2511-2518.2006

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Implication

Knockout study demonstrates embryonic lethality and severe cardiovascular defects in Calcrl-deficient mice, indicating that CLR is an essential adrenomedullin receptor in vivo.

Hydrops Fetalis, Cardiovascular Defects, and Embryonic Lethality in Mice Lacking the Calcitonin Receptor-Like Receptor Gene

Discussion

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Implication

Key Points

Cite This Study

Hydrops Fetalis, Cardiovascular Defects, and Embryonic Lethality in Mice Lacking the Calcitonin Receptor-Like Receptor Gene

Discussion

Member takes

Implication

Key Points

Cite This Study

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