New Modes of GPCR Signalling
New Modes of GPCR Signalling
New Modes of GPCR Signalling
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Embryonic Heart Growth is Regulated by Functional Antagonism<br />
Between GRIDLOCK and GATA5 in Zebrafish<br />
Haibo Jia, Sameer Chopra, Mingwei Ni, xiaoling Jiang, Xiaoqun Guan, Terri T. Ni, Sam<br />
Wells and Tao P. Zhong<br />
Departments <strong>of</strong> Medicine and Cell & Developmental Biology, Vanderbilt Medical<br />
School, Nashville, TN 37232<br />
Embryonic heart growth is revealed primarily by the proliferation <strong>of</strong> cardiomyocytes<br />
and an increase in their cell size, but the mechanisms that control heart growth during<br />
development are not well understood. In our current study we present evidence that<br />
the Hairy-related bHLH transcription factor Gridlock (Grl) negatively regulates heart<br />
growth in the zebrafish embryo. We show that a reduction in Grl activity by mutation<br />
causes an increase in myocardial gene expression and cardiomyocyte number, resulting<br />
in the development <strong>of</strong> hyperplastic hearts. Conversely, elevation <strong>of</strong> Grl activity causes<br />
differentiating cardiomyocytes to fail to divide and grow, thereby reducing the heart size<br />
in the embryo. These Grl-dependent cardiac growth effects are counterbalanced by<br />
Gata5, a transcriptional activator that promotes cardiomyocyte expansion. The<br />
antagonistic relationship between Grl and Gata5 is mediated through protein<br />
interactions that squelch the Gata5 transcriptional activity to inhibit myocardial gene<br />
expression. Hence, the opposing effects <strong>of</strong> Grl and Gata5 serve to regulate embryonic<br />
heart growth during development
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