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Articles by B. L Davidson
Total Records ( 2 ) for B. L Davidson
  L Lin , P Jiang , S Shen , S Sato , B. L Davidson and Y. Xing
 

Transposable elements (TEs) are major sources of new exons in higher eukaryotes. Almost half of the human genome is derived from TEs, and many types of TEs have the potential to exonize. In this work, we conducted a large-scale analysis of human exons derived from mammalian-wide interspersed repeats (MIRs), a class of old TEs which was active prior to the radiation of placental mammals. Using exon array data of 328 MIR-derived exons and RT–PCR analysis of 39 exons in 10 tissues, we identified 15 constitutively spliced MIR exons, and 15 MIR exons with tissue-specific shift in splicing patterns. Analysis of RNAs from multiple species suggests that the splicing events of many strongly included MIR exons have been established before the divergence of primates and rodents, while a small percentage result from recent exonization during primate evolution. Interestingly, exon array data suggest substantially higher splicing activities of MIR exons when compared with exons derived from Alu elements, a class of primate-specific retrotransposons. This appears to be a universal difference between exons derived from young and old TEs, as it is also observed when comparing Alu exons to exons derived from LINE1 and LINE2, two other groups of old TEs. Together, this study significantly expands current knowledge about exonization of TEs. Our data imply that with sufficient evolutionary time, numerous new exons could evolve beyond the evolutionary intermediate state and contribute functional novelties to modern mammalian genomes.

  S. M Ebert , A. M Monteys , D. K Fox , K. S Bongers , B. E Shields , S. E Malmberg , B. L Davidson , M Suneja and C. M. Adams
 

Prolonged fasting alters skeletal muscle gene expression in a manner that promotes myofiber atrophy, but the underlying mechanisms are not fully understood. Here, we examined the potential role of activating transcription factor 4 (ATF4), a transcription factor with an evolutionarily ancient role in the cellular response to starvation. In mouse skeletal muscle, fasting increases the level of ATF4 mRNA. To determine whether increased ATF4 expression was required for myofiber atrophy, we reduced ATF4 expression with an inhibitory RNA targeting ATF4 and found that it reduced myofiber atrophy during fasting. Likewise, reducing the fasting level of ATF4 mRNA with a phosphorylation-resistant form of eukaryotic initiation factor 2 decreased myofiber atrophy. To determine whether ATF4 was sufficient to reduce myofiber size, we overexpressed ATF4 and found that it reduced myofiber size in the absence of fasting. In contrast, a transcriptionally inactive ATF4 construct did not reduce myofiber size, suggesting a requirement for ATF4-mediated transcriptional regulation. To begin to determine the mechanism of ATF4-mediated myofiber atrophy, we compared the effects of fasting and ATF4 overexpression on global skeletal muscle mRNA expression. Interestingly, expression of ATF4 increased a small subset of five fasting-responsive mRNAs, including four of the 15 mRNAs most highly induced by fasting. These five mRNAs encode proteins previously implicated in growth suppression (p21Cip1/Waf1, GADD45, and PW1/Peg3) or titin-based stress signaling [muscle LIM protein (MLP) and cardiac ankyrin repeat protein (CARP)]. Taken together, these data identify ATF4 as a novel mediator of skeletal myofiber atrophy during starvation.

 
 
 
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