Premium
Alternative Splicing Generates Novel Fads3 Transcript in Mice
Author(s) -
Zhang Ji Yao,
Qin Xia,
Park Hikyu,
Kim Ellen,
Liu Guowen,
Kothapalli Kumar,
Brenna J Thomas
Publication year - 2015
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.29.1_supplement.743.10
Subject(s) - fads2 , exon , biology , alternative splicing , open reading frame , complementary dna , rna splicing , polyunsaturated fatty acid , gene , fatty acid desaturase , microbiology and biotechnology , genetics , rna , biochemistry , fatty acid , peptide sequence , docosahexaenoic acid
Fatty acid desaturase (FADS) gene family consists of three genes ( Fads1, Fads2 and Fads3 ). Fads1 and Fads2 catalyze critical steps in the biosynthesis of long chain polyunsaturated fatty acids (LCPUFA). Fads3 is the third member, found to have at least eight evolutionarily conserved alternative transcripts (AT), but with no clearly established function. Here we present identification of a novel Fads3 transcript in mice ( Fads3AT9 ). Our main objective is to characterize Fads3AT9 , its expression in mouse tissues and in undifferentiated and differentiated fat (white and brown) cells. Methods. Total RNA obtained from mouse tissues and fat cells were reverse‐transcribed into cDNA. The resulting cDNA was used as template for PCR‐reactions. Results. Sequencing analysis revealed complete absence of exon 2 resulting in an open reading frame of 1239 bp, encoding a putative protein of 412 aa with loss of 37 aa compared to classical Fads3 ( Fads3CS ). Fads3AT9 retains all the conserved regions characteristic of front end desaturase (cyto b5 domain and three histidine repeats). It is widely expressed in 12 different mouse tissues and fat cells, with strongest expression seen in kidney, and heart. Fads3CS had greater abundance than AT9 in all tissues. Conclusions Widespread expression patterns in mouse tissues and fat cells suggest it may play an important role in the regulation and/or biosynthesis of LCPUFA from precursors. Funding Source: NIH R01 AT007003