Líffræðifélag Íslands - biologia.is
Líffræðiráðstefnan 2019
Erindi/veggspjald / Talk/poster V12
Höfundar / Authors: Arnar Pálsson (1), Baldur Kristjánsson(1), Dagny A. Runarsdottir(1), Sudarshan Chari(2), Ian M. Dworkin(3)
Starfsvettvangur / Affiliations: 1. University of Iceland, 2. Princeton University, 3. McMaster University
Kynnir / Presenter: Arnar Pálsson
Major mutations or environmental insults can expose cryptic genetic variation that selection can operate on, and lead to restoration of fitness and phenotypes. Can cryptic genetic variation lead to the retuning or reorganized of regulatory networks after the fixation of major mutations? To address this we studied gene expression in strains of Drosophila melanogaster, that had undergone genetic perturbation and subsequent artificial selection leading to compensatory evolution of major phenotypes. Mutations in the genes net and rhomboid, known to act antagonistically during development to pattern wing veins, were introgressed into a wild type population. Replicate populations were subject to artificial selection for improved wing shape (evolved) and “natural” selection against the harmful effects of the major mutations (control). Full compensation of venation defects was achieved in the evolved flies but none was observed in control strains. We studied expression in several distinct populations: One reference (wild-type) population, two introgressed populations (net and rhomboid), and then three evolved and three control populations for each mutation. Transcriptome libraries were prepared from wing-discs of 3rd instar larvae and sequenced on Illumina HiSeq2500. The net mutation impacted expression of more genes than rhomboid, perhaps because the former is a transcription factor, whilst the latter is involved in cell signalling. We observed correlated expression of net and rhomboid, under certain conditions. Compensation of the wing phenotypes did not seem to be mediated by transcriptional restoration of these two genes, arguing against compensatory evolution of upstream factors in the same pathway. It is currently unclear whether the compensation is driven by restored expression/function of the net and rhomboid target genes, or by regulatory factors acting in parallel pathways. Interestingly, expression of some genes was altered by the compensatory selection in both backgrounds. One set of genes showed the same pattern in both net and rhomboid backgrounds, and slightly fewer genes displayed antagonistic patterns by backgrounds. Analyses of the evolved responses to permutations of several genes in overlapping or antagonizing pathways may be useful to study the modulation of regulatory networks.