Antonio Bedalov

The paper shows that chromatin architecture limits replication origin licensing capacity in budding yeast by restricting helicase loading through Isw2-dependent nucleosome repositioning.

The paper shows that proteasome-mediated degradation of misfolded proteins persists during acute glucose starvation in yeast, and nucleus-vacuole junctions support this process under metabolic stress.

This study shows that Sir2 and Fun30 regulate rDNA replication timing by controlling MCM helicase positioning and nucleosome occupancy in yeast.

The paper investigates protein quality control (PQC) in quiescent yeast cells, showing that degradation pathways like proteasomes, autophagy, and nucleus-vacuole junctions are active and required for misfolded protein clearance.

The paper identifies 1600 replication origins in S. cerevisiae by analyzing Mcm double-hexamer binding sites and shows replication activity at the most abundant sites.

This study develops a mouse model to monitor Mecp2 reactivation in neural stem cells and identifies genetic and epigenetic factors influencing reactivation of the inactive X chromosome.

The paper shows that chromosomal distribution of Mcm2-7 complexes drives replication timing across species, with exceptions like the inactive X-chromosome.