Líffræðifélag Íslands - biologia.is
Líffræðiráðstefnan 2019

Erindi/veggspjald / Talk/poster E42

Can you save a mutant? Expressional rescue of 3 major wing defects in Drosophila melanogaster

Höfundar / Authors: Baldur Kristjánsson (1), Dagný Á. Rúnarsdóttir (1), Sudarshan Chari (2), Ian Dworkin (3), Arnar Pálsson (1)

Starfsvettvangur / Affiliations: 1. University of Iceland, Reykjavík, Iceland, 2. Princeton University, Princeton, USA, 3. McMaster University, Hamilton, Canada

Kynnir / Presenter: Baldur Kristjánsson

How do phenotypes, development and regulatory networks respond to major mutations in key regulatory genes? To study the sensitivity and buffering of regulatory networks, we study tissue specific changes in strains of Drosophila melanogaster, that have undergone genetic perturbation and subsequent artificial selection leading to compensatory evolution of major phenotypes.
Mutations in vestigial (vg), net and rhomboid (rho), which affect wing development and cause wing-defects, were introgressed into a wild-type population. Replicate populations were subject to artificial selection for improved wing (evolved) and “natural” selection against the harmful effects of the major mutations (control), resulting in full and no compensation of the wing morphology. We seek to answer how gene expression is impacted by introgression of the mutants, and which expression changes correlate with rebuilt wings. In order to do so, mRNA was isolated from wing discs and sequenced on Illumina HiSeq 2500 platform. Trimming, mapping and counting was done using both Kallisto and Cutadapt – STAR – htseq-count, separately, with continuous count analysis in the R package DESeq2.
We observe strong expressional compensation in multiple genes in all compensated lineages, but little changes in control lineages. The response was strongest in vg mutants, were compensation was mediated through vg itself. We also observe changes in potential upstream, downstream and parallel agents/pathways. Our results suggest that cryptic standing genetic variation, within wild populations, can restore expression of a disrupted gene or compensate for loss of function via other mechanisms. This is likely linked to locations of genes within regulatory networks, the nature of the molecular lesions and strength of phenotypic effects.