scholarly journals Genetic architecture of natural variation in cuticular hydrocarbon composition in Drosophila melanogaster

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Lauren M Dembeck ◽  
Katalin Böröczky ◽  
Wen Huang ◽  
Coby Schal ◽  
Robert R H Anholt ◽  
...  

Insect cuticular hydrocarbons (CHCs) prevent desiccation and serve as chemical signals that mediate social interactions. Drosophila melanogaster CHCs have been studied extensively, but the genetic basis for individual variation in CHC composition is largely unknown. We quantified variation in CHC profiles in the D. melanogaster Genetic Reference Panel (DGRP) and identified novel CHCs. We used principal component (PC) analysis to extract PCs that explain the majority of CHC variation and identified polymorphisms in or near 305 and 173 genes in females and males, respectively, associated with variation in these PCs. In addition, 17 DGRP lines contain the functional Desat2 allele characteristic of African and Caribbean D. melanogaster females (more 5,9-C27:2 and less 7,11-C27:2, female sex pheromone isomers). Disruption of expression of 24 candidate genes affected CHC composition in at least one sex. These genes are associated with fatty acid metabolism and represent mechanistic targets for individual variation in CHC composition.

2019 ◽  
Vol 10 ◽  
Author(s):  
Jonathan H. Massey ◽  
Noriyoshi Akiyama ◽  
Tanja Bien ◽  
Klaus Dreisewerd ◽  
Patricia J. Wittkopp ◽  
...  

Genes ◽  
2020 ◽  
Vol 11 (2) ◽  
pp. 234 ◽  
Author(s):  
Joanne R Chapman ◽  
Maureen A Dowell ◽  
Rosanna Chan ◽  
Robert L Unckless

Dissecting the genetic basis of natural variation in disease response in hosts provides insights into the coevolutionary dynamics of host-pathogen interactions. Here, a genome-wide association study of Drosophila melanogaster survival after infection with the Gram-positive entomopathogenic bacterium Enterococcus faecalis is reported. There was considerable variation in defense against E. faecalis infection among inbred lines of the Drosophila Genetics Reference Panel. We identified single nucleotide polymorphisms associated with six genes with a significant (p < 10−08, corresponding to a false discovery rate of 2.4%) association with survival, none of which were canonical immune genes. To validate the role of these genes in immune defense, their expression was knocked-down using RNAi and survival of infected hosts was followed, which confirmed a role for the genes krishah and S6k in immune defense. We further identified a putative role for the Bomanin gene BomBc1 (also known as IM23), in E. faecalis infection response. This study adds to the growing set of association studies for infection in Drosophila melanogaster and suggests that the genetic causes of variation in immune defense differ for different pathogens.


2016 ◽  
Author(s):  
Héloïse Bastide ◽  
Jeremy D. Lange ◽  
Justin B. Lack ◽  
Yassin Amir ◽  
John E. Pool

AbstractUnraveling the genetic architecture of adaptive phenotypic divergence is a fundamental quest in evolutionary biology. In Drosophila melanogaster, high-altitude melanism has evolved in separate mountain ranges in sub-Saharan Africa, potentially as an adaptation to UV intensity. We investigated the genetic basis of this melanism in three populations using a new bulk segregant analysis mapping method. Although hundreds of genes are known to affect cuticular pigmentation in D. melanogaster, we identified only 19 distinct QTLs from 9 mapping crosses, with several QTL peaks being shared among two or all populations. Surprisingly, we did not find wide signals of genetic differentiation (Fst) between lightly and darkly pigmented populations at these QTLs, in spite of the pronounced phenotypic difference in pigmentation. Instead, we found small numbers of highly differentiated SNPs at the probable causative genes. A simulation analysis showed that these patterns of polymorphism are consistent with selection on standing genetic variation (leading to “soft sweeps“). Our results thus support a role for oligogenic selection on standing genetic variation in driving parallel ecological adaptation.


2020 ◽  
Vol 10 (4) ◽  
pp. 1247-1260 ◽  
Author(s):  
Louis P. Watanabe ◽  
Cameron Gordon ◽  
Mina Y. Momeni ◽  
Nicole C. Riddle

Exercise is recommended by health professionals across the globe as part of a healthy lifestyle to prevent and/or treat the consequences of obesity. While overall, the health benefits of exercise and an active lifestyle are well understood, very little is known about how genetics impacts an individual’s inclination for and response to exercise. To address this knowledge gap, we investigated the genetic architecture underlying natural variation in activity levels in the model system Drosophila melanogaster. Activity levels were assayed in the Drosophila Genetics Reference Panel fly strains at baseline and in response to a gentle exercise treatment using the Rotational Exercise Quantification System. We found significant, sex-dependent variation in both activity measures and identified over 100 genes that contribute to basal and induced exercise activity levels. This gene set was enriched for genes with functions in the central nervous system and in neuromuscular junctions and included several candidate genes with known activity phenotypes such as flightlessness or uncoordinated movement. Interestingly, there were also several chromatin proteins among the candidate genes, two of which were validated and shown to impact activity levels. Thus, the study described here reveals the complex genetic architecture controlling basal and exercise-induced activity levels in D. melanogaster and provides a resource for exercise biologists.


2016 ◽  
Vol 113 (43) ◽  
pp. E6620-E6629 ◽  
Author(s):  
Mary Anna Carbone ◽  
Akihiko Yamamoto ◽  
Wen Huang ◽  
Rachel A. Lyman ◽  
Tess Brune Meadors ◽  
...  

Senescence, i.e., functional decline with age, is a major determinant of health span in a rapidly aging population, but the genetic basis of interindividual variation in senescence remains largely unknown. Visual decline and age-related eye disorders are common manifestations of senescence, but disentangling age-dependent visual decline in human populations is challenging due to inability to control genetic background and variation in histories of environmental exposures. We assessed the genetic basis of natural variation in visual senescence by measuring age-dependent decline in phototaxis using Drosophila melanogaster as a genetic model system. We quantified phototaxis at 1, 2, and 4 wk of age in the sequenced, inbred lines of the Drosophila melanogaster Genetic Reference Panel (DGRP) and found an average decline in phototaxis with age. We observed significant genetic variation for phototaxis at each age and significant genetic variation in senescence of phototaxis that is only partly correlated with phototaxis. Genome-wide association analyses in the DGRP and a DGRP-derived outbred, advanced intercross population identified candidate genes and genetic networks associated with eye and nervous system development and function, including seven genes with human orthologs previously associated with eye diseases. Ninety percent of candidate genes were functionally validated with targeted RNAi-mediated suppression of gene expression. Absence of candidate genes previously implicated with longevity indicates physiological systems may undergo senescence independent of organismal life span. Furthermore, we show that genes that shape early developmental processes also contribute to senescence, demonstrating that senescence is part of a genetic continuum that acts throughout the life span.


2020 ◽  
Vol 287 (1928) ◽  
pp. 20200057
Author(s):  
Allison Jaffe ◽  
Madeline P. Burns ◽  
Julia B. Saltz

Social interactions can influence the expression and underlying genetic basis of many traits. Yet, empirical investigations of indirect genetic effects (IGEs) and genotype-by-genotype epistasis—quantitative genetics parameters representing the role of genetic variation in a focal individual and its interacting partners in producing the observed trait values—are still scarce. While it is commonly observed that an individual's traits are influenced by the traits of interacting conspecifics, representing social plasticity, studying this social plasticity and its quantitative-genetic basis is notoriously challenging. These challenges are compounded when individuals interact in groups, rather than (simpler) dyads. Here, we investigate the genetic architecture of social plasticity for exploratory behaviour, one of the most intensively studied behaviours in recent decades. Using genotypes of Drosophila simulans , we measured genotypes both alone, and in social groups representing a mix of two genotypes. We found that females adjusted their exploratory behaviour based on the behaviour of others in the group, representing social plasticity. However, the direction of this plasticity depended on the identity of group members: focal individuals were more likely to emerge from a refuge if group members who were the same genotype as the focal remained inside for longer. By contrast, focal individuals were less likely to emerge from a refuge if partner-genotype group members remained inside for longer. Exploratory behaviour also depended on the identities of both genotypes that composed the group. Together, these findings demonstrate genotype-by-genotype epistasis for exploratory behaviour both within and among groups.


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