Skip Navigation


Cardiovascular Research Advance Access first published online on June 25, 2008
This version [Corrected Proof] published online on July 14, 2008

Cardiovascular Research, doi:10.1093/cvr/cvn177
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Supplementary Data
Right arrow All Versions of this Article:
cvn177v2    most recent
cvn177v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Zhao, L.
Right arrow Articles by Meng, A.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhao, L.
Right arrow Articles by Meng, A.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Heart-specific isoform of tropomyosin4 is essential for heartbeat in zebrafish embryos

Long Zhao1,{dagger}, Xinyi Zhao1,{dagger}, Tian Tian1,{dagger}, Quanlong Lu2, Nirma Skrbo-Larssen1, Di Wu1, Zheng Kuang1, Xiaofeng Zheng1, Yanchao Han1, Shuyan Yang1, Chuanmao Zhang2 and Anming Meng1,*

1 Protein Science Laboratory of the Ministry of Education, Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing 100084, People's Republic of China
2 Laboratory of Cell Proliferation and Differentiation of the Ministry of Education, College of Life Sciences, Peking University, Beijing 100871, People's Republic of China

* Corresponding author. Tel: +86 10 62772256; fax: +86 10 62794401. E-mail address: mengam{at}mail.tsinghua.edu.cn

Aims: Tropomyosin (Tpm) proteins, encoded by four Tpm genes (Tpm1–4), are associated with the stabilization of the F-actin filaments and play important roles in modulating muscle contraction. So far, little is known about Tpm4 function in embryonic heart development and its involvement in the cardiovascular diseases. In this study, we investigated functions of different isoforms of tpm4 in embryonic heartbeat in zebrafish.

Methods and results: The transgenic zebrafish line, T2EGEZ8, was generated by insertion of a Tol2 transposon gene trap vector, and homozygous mutants (T2EGEZ8m/m) of this line showed failure of embryonic heartbeat without other detectable phenotypes. Observation by transmission electron microscopy revealed that the ventricular myocytes of mutant fish contained fewer, disorganized myofibrillar filaments. The transposon genome in T2EGEZ8 fish was found by thermal asymmetric interlaced-polymerase chain reaction (TAIL-PCR) and reverse transcription-polymerase chain reaction to have inserted into the ninth intron of the tpm4 locus, which resulted in production of Tpm4-GFP fusion proteins and loss of normal transcripts tpm4-tv1 and tpm4-tv2. Whole-mount in situ hybridization indicated that tpm4-tv1, encoding a peptide of 284 residues, is specifically expressed in the heart of zebrafish embryos, while tpm4-tv2, encoding a peptide of 248 residues, is mainly present in the vasculature but absent in the heart. Knockdown of tpm4-tv1 and tpm4-tv2 within wild-type embryos led to the failure of heartbeat, which could be rescued by coinjection with tpm4-tv1 mRNA but not with tpm4-tv2 mRNA.

Conclusion: Tpm4-tv1 is a heart-specific isoform of Tpm4 and is essential for heartbeat in zebrafish embryos.

KEYWORDS Zebrafish; Heart; Tropomyosin; Transposon; Thin filament


Time for primary review: 34 days

{dagger} These authors contributed equally to this work.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.