Resumen del trabajo presentado en el Spanish Meiosis Meeting 2021, celebrado de forma virtual del 6 al 8 de Julio
Meiotic recombination begins with the regulated production of Double Strand Breaks (DSBs) at specific regions of the genome known as hotspots. DSBs are catalysed by the Spo11 complex, which in budding yeast is formed by ten proteins. Pre-meiotic DNA-replication, transcription, epigenetic modifications and chromosome structure strongly influence where and when those hotspots are expressed globally. Nonetheless, little is known about the relative timing of expression between different hotspots. It has been shown that different mutations in DNA repair affect how DSBs are distributed genome-wide, particularly the sae2/rad50S class of mutations as opposed to the dmc1-type of mutants. Furthermore, Tel1-dependent phosphorylation of Rec114, a regulator of Spo11, modulates total levels of DSBs. Rec114 mutants where these phosphorylation sites were modified, displayed different hotspot preference by Spo11. Analysing datasets from DSB maps of several of these mutant combinations allowed us to predict the existence of two separate types of DSB hotspots in budding yeast. Here, using a physical assay and biostatistics, I will present some examples of hotspots from different chromosomes displaying different timing in DSB initiation as initially predicted by our model, whereas others remained inconclusive. Overall, our results stablish the basis to better predict timing of programmed DSB formation in meiosis and it provides with a mechanistic explanation for the existence of a spatio-temporal network controlling their genome-wide distribution.