Not haploid after all: the patterns and processes generating somatic mutations across honey bee (Apis mellifera) males

Monday, November 14, 2022

12:06 PM – 12:18 PM PT

Location: Vancouver Convention Centre, Meeting Room 220

Presenting Author(s)

Riley R. Shultz (she/her/hers)

Graduate Student
Purdue University
West Lafayette, Indiana

Co-Author(s)

BH

Brock Harpur

Assistant Professor
Purdue University
West Lafayette, Indiana

Haploid organisms are susceptible to any deleterious alleles inherited from their parent or that arise over their lifetime. The latter, which include somatic mutations, originate from both exogenous mutagens (e.g. UV radiation) and endogenous processes (e.g. DNA replication). The fitness impact of somatic mutations can be high and may limit reproductive success. This can be especially important for haplodiploids where males are typically haploid and thus are impacted by recessive deleterious mutations. Further, in haplodiploid bees, additional features such as the process of endoreplication, may contribute to the rapid gain of somatic mutations. Other factors such as exposure to oxidative stress and aging further contribute to the accumulation of somatic mutations. We lack fundamental knowledge about the rates and distribution of somatic mutations in haplodiploids and how they may impact fitness. I have developed a unique experimental design in honey bees to detect somatic mutations and directly identify patterns across tissues and identify processes leading to somatic mutations. I began to investigate the role of ploidy in the accumulation of somatic mutations by first quantifying the ploidy of the brain, muscle, midgut, and reproductive systems of individual drones. From there, I used long- and short-read technologies to sequence tissue-specific genomes. My preliminary data suggests that honey bee drones have tissue-specific mutations in gene regions and experience high rates of somatic mutations.