Meeting Abstract

P3.159  Friday, Jan. 6  Transcriptome analysis of the regulatory mechanisms of intestinal response for the Burmese python SECOR, Stephen M.*; CASTOE, Todd A.; POLLOCK, David D.; University of Alabama; University of Colorado School of Medicine; University of Colorado School of Medicine ssecor@biology.as.ua.edu

Snakes that feed relatively infrequently in the wild experience unprecedented magnitudes of regulatory responses with the onset and completion of digestion. For the small intestine, feeding triggers rapid upregulation of intestinal nutrient uptake and hydrolase activities, and cellular hypertrophy that is accompanied by 5-fold lengthening of the microvilli. These responses are reversed once digestion has completed. To examine potential molecular mechanisms underlying intestinal regulation for these snakes, we employed high-throughput Illumina RNA-Seq transcriptome profiling to examine differential expression of genes for fasted and fed Burmese pythons (Python molurus). We constructed and sequenced 33 multiplexed cDNA libraries from intestines sampled from pythons fasted and at 6 h, 12 h, 1 d, 4 d, and 10 d postfeeding. Reads were co-assembled de novo with other python cDNA data, yielding ~150,000 contigs > 250 bp that were annotated based on similarity to Anolis, chicken and human genes. Using these contings as a reference transcriptome, transcript abundances where estimated for each intestinal library. Of the more than 12,000 intestinal transcripts, 2,700 were upregulated by ≥10-fold after feeding. Transcripts showing extreme dynamics (≥300-fold changes) include those for the microvillus protein ezrin, brush border aminopeptidases and amino acid transporters, metabolic pathways, stress response, and calcium binding. This study demonstrates that massive transcriptional responses accompany the extensive physiological remodeling of the python’s intestine with feeding. Here we provide preliminary evidence identifying the molecular mechanisms that underlie the phenotypic transitions in intestinal form and function.