Five pillars of centromeric chromatin in fungal pathogens

Abstract

A centromere is classically defined as the primary constriction on a metaphase chromosome [1] that holds the sister chromatids together, binds to spindle microtubules, and brings about their separation during anaphase. Despite having a conserved and essential function, centromeres are among the fastest evolving DNA sequence loci in eukaryotic genomes [2]. With the advent of molecular biology techniques, centromeres could be mapped and sequenced in a large number of fungal species. The length of centromere DNA in fungi is found to be highly variable, classifying them as point (<400 bp), short regional (>400 bp, <20 kb), and large regional (>20 kb) [3]. Such diversity is achieved by different regulatory factors that have overlapping functions required for loading of the centromere-specific histone H3 variant centromere protein A/chromosome segregation 4(CENP-A/Cse4) to DNA to define centromere identity. Although genetic and epigenetic mechanisms of centromere formation across eukaryotes are largely conserved, there are examples of molecular innovation and genetic improvisation that help fungal species to maintain their ploidy across generations. In this review, we highlight five such genetic and epigenetic factors that define centromere identity in pathogenic fungi.