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Gene expression analyses of a regenerative cardiac model system in Ciona intestinalis
Author(s) -
Manning Caitlin LaShea,
Pardhanani Pooja,
Barth Jeremy,
EvansAnderson Heather
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.529.1
Subject(s) - ciona intestinalis , ciona , biology , gene , in silico , microarray analysis techniques , regeneration (biology) , microarray , gene expression profiling , genetics , model organism , transcriptome , gene expression , microbiology and biotechnology , computational biology
Ciona intestinalis is a useful invertebrate animal model system for studying the role of evolutionarily conserved genes among Chordates. In contrast to most vertebrates, Ciona hearts have the capacity for regeneration throughout their lifespan. An injury model system was used to stimulate regeneration in Ciona hearts. In order to identify genes that are involved in regeneration of the Ciona heart, microarray analysis was conducted on RNA from adult hearts with normal or damaged myocardium using custom Affymetrix GeneChips. Initial results indicate significant changes in the expression of 223 genes in hearts damaged by ligation in comparison to control hearts (fold change >;2, p<0.01, Student's t‐test) with limited false discovery (5.8%). Among these 223 genes, 117 have known orthologs to vertebrates, of which 68 genes were up‐regulated and 49 genes were down‐regulated. Altered orthologous genes were validated by RT‐PCR. In addition, expression patterns of genes identified in the microarray study are currently being identified via in situ hybridization in juvenile and adult Ciona hearts. Genes of interest include: ciFGF 9/16/20, ciFoxO, and ciFoxP. In combination, these studies will help to elucidate the genetic basis of myocardial regeneration in Ciona and provide further insight into the role of orthologous genes in the regulation of cardiac myocyte proliferation. Grant Funding Source : NIH R15 Area Grant