Evaluación de la expresión diferencial de hotspots de roturas de doble hebra de ADN y su regulación por la respuesta daño genómico en la meiosis de Saccharomyces cerevisiae

Abstract

During meiosis two cellular divisions are preceded by a single round of genome replication. In Saccharomyces cerevisiae, for meiosis to being correctly produced, homologous chromosomes must pair, synapse and recombine.Recombination has its origin in double strand breaks (DSBs) catalyzed by the Spo11 complex. They are spatiotemporally regulated by Mec1 and Tel1 kinases. These kinases phosphorylate residues known as (S/T)Q: serines and threonines followed by a glutamine in the aminoacidic sequence.It has been established that the phosphorylation by Tel1 of Rec114, one of the components of the Spo11 complex, leads to the inhibition of DSBs formation. When all the (S/T)Q residues of Rec114 are substituted by phosphomimetic aminoacids, a delay in the production of double strand breaks occur. This delay entails a reduction in the quantity of DSBs when it occurs in rad50S/sae2Δ genetics backgrounds. This reduction in DSBs is similar to the one seen when DSBs production is delayed by delaying DNA replication in rad50S/sae2Δ backgrounds. However, this reduction does not occur in wild type backgrounds or dmc1Δ, being the Dmc1 protein a meiotic recombinase.It has also been reported that the quantity of described hotspots in rad50S/sae2Δ backgrounds is lesser than the quantity of hotspots described in dmc1Δ backgrounds. One possible cause for this is that the hotspots that are not expressed in rad50S/sae2Δ strains may be highly regulated by Rec114. The rest of the hotspots, which are expressed under these conditions, would be less regulated by this protein...