Modulation of cardiac growth and development by HOP, an unusual homeodomain protein

Chong Hyun Shin; Zhi Ping Liu; Robert Passier; Chun Li Zhang; Da Zhi Wang; Thomas M. Harris; Hiroyuki Yamagishi; James A. Richardson; Geoffrey Childs; Eric N. Olson

doi:10.1016/S0092-8674(02)00933-9

Modulation of cardiac growth and development by HOP, an unusual homeodomain protein

Chong Hyun Shin, Zhi Ping Liu, Robert Passier, Chun Li Zhang, Da Zhi Wang, Thomas M. Harris, Hiroyuki Yamagishi, James A. Richardson, Geoffrey Childs, Eric N. Olson

Pathology

Research output: Contribution to journal › Article › peer-review

209 Scopus citations

Abstract

We have discovered an unusual homeodomain protein, called HOP, which is comprised simply of a homeodomain. HOP is highly expressed in the developing heart where its expression is dependent on the cardiac-restricted homeodomain protein Nkx2.5. HOP does not bind DNA and acts as an antagonist of serum response factor (SRF), which regulates the opposing processes of proliferation and myogenesis. Mice homozygous for a HOP null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes. We propose that HOP modulates SRF activity during heart development; its absence results in an imbalance between cardiomyocyte proliferation and differentiation with consequent abnormalities in cardiac morphogenesis.

Original language	English (US)
Pages (from-to)	725-735
Number of pages	11
Journal	Cell
Volume	110
Issue number	6
DOIs	https://doi.org/10.1016/S0092-8674(02)00933-9
State	Published - Sep 20 2002

ASJC Scopus subject areas

General Biochemistry, Genetics and Molecular Biology

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title = "Modulation of cardiac growth and development by HOP, an unusual homeodomain protein",

abstract = "We have discovered an unusual homeodomain protein, called HOP, which is comprised simply of a homeodomain. HOP is highly expressed in the developing heart where its expression is dependent on the cardiac-restricted homeodomain protein Nkx2.5. HOP does not bind DNA and acts as an antagonist of serum response factor (SRF), which regulates the opposing processes of proliferation and myogenesis. Mice homozygous for a HOP null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes. We propose that HOP modulates SRF activity during heart development; its absence results in an imbalance between cardiomyocyte proliferation and differentiation with consequent abnormalities in cardiac morphogenesis.",

author = "Shin, {Chong Hyun} and Liu, {Zhi Ping} and Robert Passier and Zhang, {Chun Li} and Wang, {Da Zhi} and Harris, {Thomas M.} and Hiroyuki Yamagishi and Richardson, {James A.} and Geoffrey Childs and Olson, {Eric N.}",

note = "Funding Information: We thank Jon Epstein for sharing results prior to publication, Richard Harvey for Nkx2.5 mutant mice, and Robert Schwartz, Yukio Hiroi, and Issei Komuro for reagents. We are grateful to Deepak Srivastava for comments on the paper, Norbert Frey for echocardiography Yin-Chai Cheals for blastocyst injections, and John Shelton for his assistance with fluorescence microscopy. Supported by grants from NIH, The D.W. Reynolds Center for Clinical Cardiovascular Research, and the McGowan Charitable Fund to E.N.O. ",

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doi = "10.1016/S0092-8674(02)00933-9",

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T1 - Modulation of cardiac growth and development by HOP, an unusual homeodomain protein

AU - Shin, Chong Hyun

AU - Liu, Zhi Ping

AU - Passier, Robert

AU - Zhang, Chun Li

AU - Wang, Da Zhi

AU - Harris, Thomas M.

AU - Yamagishi, Hiroyuki

AU - Richardson, James A.

AU - Childs, Geoffrey

AU - Olson, Eric N.

N1 - Funding Information: We thank Jon Epstein for sharing results prior to publication, Richard Harvey for Nkx2.5 mutant mice, and Robert Schwartz, Yukio Hiroi, and Issei Komuro for reagents. We are grateful to Deepak Srivastava for comments on the paper, Norbert Frey for echocardiography Yin-Chai Cheals for blastocyst injections, and John Shelton for his assistance with fluorescence microscopy. Supported by grants from NIH, The D.W. Reynolds Center for Clinical Cardiovascular Research, and the McGowan Charitable Fund to E.N.O.

PY - 2002/9/20

Y1 - 2002/9/20

N2 - We have discovered an unusual homeodomain protein, called HOP, which is comprised simply of a homeodomain. HOP is highly expressed in the developing heart where its expression is dependent on the cardiac-restricted homeodomain protein Nkx2.5. HOP does not bind DNA and acts as an antagonist of serum response factor (SRF), which regulates the opposing processes of proliferation and myogenesis. Mice homozygous for a HOP null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes. We propose that HOP modulates SRF activity during heart development; its absence results in an imbalance between cardiomyocyte proliferation and differentiation with consequent abnormalities in cardiac morphogenesis.

AB - We have discovered an unusual homeodomain protein, called HOP, which is comprised simply of a homeodomain. HOP is highly expressed in the developing heart where its expression is dependent on the cardiac-restricted homeodomain protein Nkx2.5. HOP does not bind DNA and acts as an antagonist of serum response factor (SRF), which regulates the opposing processes of proliferation and myogenesis. Mice homozygous for a HOP null allele segregate into two phenotypic classes characterized by an excess or deficiency of cardiac myocytes. We propose that HOP modulates SRF activity during heart development; its absence results in an imbalance between cardiomyocyte proliferation and differentiation with consequent abnormalities in cardiac morphogenesis.

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SP - 725

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JO - Cell

JF - Cell

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Modulation of cardiac growth and development by HOP, an unusual homeodomain protein

Abstract

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