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BMC Genomics  2001 

Genomic organization of Tropomodulins 2 and 4 and unusual intergenic and intraexonic splicing of YL-1 and Tropomodulin 4

DOI: 10.1186/1471-2164-2-7

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Abstract:

In this study, we determined the genomic structure of TMOD2 and TMOD4 and found the organization of both genes to be similar. Sequence analysis of TMOD2 revealed no mutations or polymorphisms in ALS5 patients or controls. Interestingly, we discovered that another gene, YL-1, intergenically splices into TMOD4. YL-1 encodes six exons, the last of which is 291 bp from a 5' untranslated exon of TMOD4. We used 5' RACE and RT-PCR from TMOD4 to identify several intergenic RACE products. YL-1 was also found to undergo unconventional splicing using non-canonical splice sites within exons (intraexonic splicing) to produce several alternative transcripts.The genomic structure of TMOD2 and TMOD4 have been delineated. This should facilitate future mutational analysis of these genes. In addition, intergenic splicing at TMOD4/YL-1 was discovered, demonstrating yet another level of complexity of gene organization and regulation.Tropomodulins are the vertebrate proteins that cap the pointed ends of filamentous actin [1]. The first tropomodulin (TMOD) gene was cloned by Sung and colleagues (1992) from a fetal liver library. Three additional family members have been identified in humans, and TMOD homologs have been identified in mouse, rat, chick, Drosophila, and C. elegans[2-8]. Expression patterns vary extensively: Tropomodulin 3 (TMOD3) is ubiquitous; Tropomodulin 1 (TMOD1) is widespread in heart, muscle, brain, lens, erythrocytes, and arterioles; Tropomodulin 2 (TMOD2) is restricted to neuronal tissue; Tropomodulin 4 (TMOD4). is expressed in skeletal muscle, with a less abundant ~7 kb transcript expressed in both skeletal and cardiac muscle [8]. Whereas tropomodulins or the Arp 2/3 complex cap the pointed end of actin filaments, the barbed end can be capped by CapZ, α, β, and γ adducins as well as gelsolin [9-11]. Control of thin filament length is critical for maintaining proper sarcomere function and length[12]. Inhibition of Tmod1's capping activity – either by using an antibod

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