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Abstract
Resistin (encoded by Retn) was previously identified in rodents as a hormone associated with diabetes; however human resistin is instead linked to inflammation. Resistin is a member of a small gene family that includes the resistin-like peptides (encoded by Retnl genes) in mammals. Genomic searches of available genome sequences of diverse vertebrates and phylogenetic analyses were conducted to determine the size and origin of the resistin-like gene family. Genes encoding peptides similar to resistin were found in Mammalia, Sauria, Amphibia, and Actinistia (coelacanth, a lobe-finned fish), but not in Aves or fish from Actinopterygii, Chondrichthyes, or Agnatha. Retnl originated by duplication and transposition from Retn on the early mammalian lineage after divergence of the platypus, but before the placental and marsupial mammal divergence. The resistin-like gene family illustrates an instance where the locus of origin of duplicated genes can be identified, with Retn continuing to reside at this location. Mammalian species typically have a single copy Retn gene, but are much more variable in their numbers of Retnl genes, ranging from 0 to 9. Since Retn is located at the locus of origin, thus likely retained the ancestral expression pattern, largely maintained its copy number, and did not display accelerated evolution, we suggest that it is more likely to have maintained an ancestral function, while Retnl, which transposed to a new location, displays accelerated evolution, and shows greater variability in gene number, including gene loss, likely evolved new, but potentially lineage-specific, functions.
Highlights
Resistin (Retn) was first identified in mice about 15 years ago, where it was identified as “adipose-tissue-specific secretory factor” (ADSF) [1] and “found in the inflammatory zone 3” (FIZZ3) [2], but acquired the name Resistin as it was associated with “resistance to insulin” [3]
Our searches of the genomes of 116 vertebrate species that were available in the Ensembl and NCBI genome databases in December 2014 resulted in the identification of 206 Retn or Retnl genes from a total of 84 species, of which 136 possessed intact coding sequences that encoded potentially functional proteins
Since Retnl transposed to a new genomic location, its expression pattern may have changed due to the loss of regulatory elements that were not duplicated with the gene or due to the gain of new regulatory elements from its new genomic neighborhood
Summary
Resistin (Retn) was first identified in mice about 15 years ago, where it was identified as “adipose-tissue-specific secretory factor” (ADSF) [1] and “found in the inflammatory zone 3” (FIZZ3) [2], but acquired the name Resistin as it was associated with “resistance to insulin” [3]. When human resistin (RETN) was characterized, it was found to be expressed in macrophages rather than adipose tissue [4], and the levels of PLOS ONE | DOI:10.1371/journal.pone.0130188. Evolution of Resistin circulating resistin are associated with inflammation rather than the amount of adipose tissue [5]. Further studies over the past 10 years have confirmed that rodent and human resistin have distinct expression patterns, and while the circulating levels of resistin may be increased in diabetes, these increases are likely mediated by different mechanisms in each species [6,7,8]. In addition to diabetes, elevated levels of resistin are associated with other human diseases, including cardiovascular diseases such as arteriosclerosis and heart failure [8,13,14] and cancer [9]
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