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Volume 272, Number 51, Issue of December 19, 1997 pp. 32115-32120

Tissue-specific Alternative Splicing of Ascidian Troponin I Isoforms
REDESIGN OF A PROTEIN ISOFORM-GENERATING MECHANISM DURING CHORDATE EVOLUTION

(Received for publication, July 29, 1997, and in revised form, October 2, 1997)

Darren W. MacLean , Thomas H. Meedel ^§ and Kenneth E. M. Hastings

From the  Montreal Neurological Institute and Biology Department, McGill University, Montreal, Quebec, Canada H3A 2B4 and ^§ Department of Biology, Rhode Island College, Providence, Rhode Island 02908

In vertebrates, troponin I (TnI) exists as shorter and longer isoforms encoded by distinct genes expressed in skeletal and cardiac muscle, respectively. We report that the protochordate ascidian Ciona intestinalis expresses a homologous set of shorter and longer TnI isoforms in body wall muscle and heart, respectively. The heart-specific segment of the ascidian longer TnI isoform shares several sequence features with vertebrate cardiac TnI but lacks the protein kinase A phosphorylation sites implicated in sympatho-adrenal control of cardiac function. In contrast with vertebrates, the ascidian longer and shorter TnI isoforms are produced from a single gene by tissue-specific alternative RNA splicing; remarkably, the molecular mechanism of TnI isoform generation has been entirely reworked during ascidian/vertebrate evolution. Because alternative splicing is the more probable chordate ancestral condition, the long/cardiac versus short/somatic muscle pattern of TnI isoforms likely existed before the occurrence of the gene duplication events that created the vertebrate TnI gene family. Thus, gene duplication was apparently not the primary engine of isoform diversity in this aspect of TnI gene family evolution; rather, it simply provided an alternative (transcriptional) means of maintaining a previously established system of isoform diversity and tissue specificity based on alternative RNA splicing.

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