Gene dose compensation mechanism in Xenopus laevis

SANCHEZ R.S.; LAZARTE M.A.; SÁNCHEZ S.S.

Tafi del Valle, Tucumán, Argentina

Congreso; XXXV Annual Scientific Meeting Tucumán Biology Association; 2018

Asociacion de Biologia de Tucumán

Throughout evolution, polyploidization events have shaped various eukaryotic genomes. Polyploidy provides raw material for evolutionary diversification because gene duplicates can support new functions. However, the component subgenomes of a polyploid must cooperate to mediate potential incompatibilities of gene dose, regulatory controls and protein?protein interactions. Redundant functional elements in a polyploid are expected to rapidly revert to single copies through the fixation of disabling mutations and/or loss unless prevented by neofunctionalization, subfunctionalization, or selection for gene dose. Recent studies have demonstrated that X. laevis is an allotetraploidorganism whose genome is partitioned into two distinct homoeologous subgenomes (L and S) which, despite sharing the same nucleus the subgenomes, do not recombine with each other and have evolved asymmetrically. In this work, we cloned and functionally characterization the uncx.S and uncx.L transcription factors of X. laevis. The comparative analysis of the protein sequences showed that uncx.L gene is truncated, lacking the C-terminal domain (similar to dominant negative). Through the in situ hybridization technique, we found that these homologous pairs are expressed in the sclerotome and in the pharyngeal pouches; additionally, uncx.S is also expressed in the pronephros. On the other hand, we conducted experiments of gain and loss of function of uncx homologs. In these assays we demonstrated that both uncx genes play an important role in sclerotome development and showed a novel mechanism of regulation of gene dose in which uncx.L antagonizes with uncx.S function, possibly through a competitive inhibition of binding to target genes.