Cloning, mRNA expression and transcriptional regulation of five retinoid X receptor subtypes in yellow catfish Pelteobagrus fulvidraco by insulin

Gen Comp Endocrinol. 2016 Jan 1:225:133-141. doi: 10.1016/j.ygcen.2015.10.010. Epub 2015 Nov 11.

Abstract

Retinoid X receptors (RXRs) are members of the nuclear receptor superfamily and mediate development, reproduction, homeostasis and cell differentiation processes in vertebrates. In this study, full-length cDNA sequences of five rxr subtypes from yellow catfish Pelteobagrus fulvidraco were cloned. Their mRNA expression patterns in different tissues and transcriptional regulation by insulin were determined. Five P. fulvidraco rxr (Pf-rxr) subtypes differed in the length of cDNA sequence and the open reading frame, but shared the similar domain structures as in typical nuclear receptors. Phylogenetic analysis revealed that the five Pf-rxr subtypes were paralogous genes, and that Pf-rxrβa and Pf-rxrβb had arisen during a teleost-specific genome duplication event. Five subtypes of Pf-rxr were detected in all the tested tissues. Overlapping and distinct expression patterns were found for different Pf-rxr subtypes, suggesting functional redundancy and divergence of these duplicates. Intraperitoneal insulin injection and incubation reduced the mRNA expression of Pf-rxrgb, but not other subtypes, in the liver and hepatocytes of P. fulvidraco, respectively, suggesting that Pf-rxrgb is the dominant rxr subtype involved in the insulin signaling pathway in P. fulvidraco.

Keywords: Gene expression profiling; Insulin; Molecular cloning; Pelteobagrus fulvidraco; Retinoid X receptors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Catfishes / genetics
  • Catfishes / metabolism*
  • Cloning, Molecular
  • Gene Expression Regulation / drug effects*
  • Hepatocytes / drug effects
  • Hepatocytes / metabolism
  • Insulin / pharmacology*
  • Liver / drug effects
  • Liver / metabolism
  • Phylogeny
  • RNA, Messenger / genetics
  • Receptors, Cytoplasmic and Nuclear / metabolism
  • Retinoid X Receptors / genetics
  • Retinoid X Receptors / metabolism*
  • Transcription, Genetic / drug effects*

Substances

  • Insulin
  • RNA, Messenger
  • Receptors, Cytoplasmic and Nuclear
  • Retinoid X Receptors