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Calreticulin is essential for cardiac development.

N Mesaeli¹, K Nakamura, E Zvaritch

¹Medical Research Council Group in Molecular Biology of Membranes, Department of Biochemistry, University of Alberta, Canada.

The Journal of Cell Biology

|March 23, 1999

Summary

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Calreticulin gene disruption in mice causes omphalocele and cardiac defects. Calreticulin is crucial for cardiovascular development and calcium homeostasis.

Area of Science:

Molecular Biology
Developmental Biology
Cardiovascular Biology

Background:

Calreticulin (CRT) is a Ca2+ binding protein in the endoplasmic reticulum lumen.
CRT is involved in diverse cellular functions, including Ca2+ homeostasis and gene regulation.

Purpose of the Study:

To investigate the physiological function of calreticulin using gene targeting.
To elucidate calreticulin's role in cardiac development and Ca2+ signaling.

Main Methods:

Generation of calreticulin knockout (crt-/-) mice.
Analysis of cardiac morphology and function in knockout mice.
Investigation of Ca2+ signaling and nuclear import in calreticulin-deficient cells.

Main Results:

Related Experiment Videos

Homozygous calreticulin disruption resulted in omphalocele and decreased ventricular wall thickness.
Calreticulin gene expression is highly activated in the developing cardiovascular system.
Calreticulin deficiency impaired bradykinin-induced Ca2+ release and NF-AT3 nuclear import.

Conclusions:

Calreticulin plays a critical role in early cardiac development and cardiovascular system formation.
Calreticulin is essential for maintaining intracellular Ca2+ homeostasis.
Calreticulin functions within the Ca2+/calcineurin/NF-AT/GATA-4 pathway during cardiac development.