Bonita J. Brewer

The paper investigates the mcm4Chaos3 mutation in yeast, showing it causes genome instability by impairing specific centromere-proximal origins.

The paper investigates rDNA instability in aging yeast, identifying new forms of instability beyond ERCs that contribute to lifespan variability.

The paper identifies a mechanism of gene amplification in yeast involving microhomology-mediated break-induced replication (mmBIR) at telomeres, leading to tandem duplication of chromosomal ends.

The paper investigates how rDNA copy number variation affects yeast fitness under different environmental conditions and finds that higher copy numbers improve fitness in stress conditions.

The paper proposes a unifying mechanism, ODIRA, to explain the origins of human inverted copy number variants and their role in both inherited syndromes and cancer.

The paper identifies a replication error mechanism called ODIRA that generates inverted copy number variants through template switching at replication forks, using yeast as a model system.

The paper identifies de novo telomere addition at a hotspot near SUL1 in yeast under sulfate-limiting conditions, stabilizing linear amplicons and contributing to genomic plasticity.

The paper shows that reducing rDNA copy number in S. cerevisiae changes its replication timing, delays genome replication, and links rDNA to cell cycle control via Cdc14p sequestration.

This study shows that Sld2 and Sld3 abundance primarily affect origin efficiency in yeast replication, not firing time, using auxin-induced degradation.

This study edits rDNA replication origins in yeast using CRISPR/Cas9, revealing growth and lifespan consequences of such modifications.