scholarly journals Evolution of plasticity in response to ethanol between sister species with different ecological histories (Drosophila melanogaster and D. simulans)

2018 ◽  
Author(s):  
Sarah A. Signor

AbstractThe contribution of phenotypic plasticity to adaptation is contentious, with contradictory empirical support for its role in evolution. Here I investigate the possibility that phenotype plasticity has contributed to adaptation to a novel resource. If phenotype plasticity contributes to adaptation, it is thought to evolve in a process termed genetic accommodation. Under this model, the initial response to the environment is widely variable due to cryptic genetic variation, which is then refined by selection to a single adaptive response. I examine the role of phenotypic plasticity in adaptation here by comparing two species of Drosophila that differ in their adaptation to ethanol (Drosophila melanogaster and D. simulans). Both species are human commensals with a recent cosmopolitan expansion, but only D. melanogaster is adapted to ethanol exposure. I measure phenotype plasticity in response to ethanol with gene expression and an approach that combines information about expression and alternative splicing. I find evidence for adaptation to ethanol through genetic accommodation, suggesting that the evolution of phenotype plasticity contributed to the ability of D. melanogaster to exploit a novel resource. I also find evidence that alternative splicing may be more important for the adaptive response to ethanol than overall changes in exon expression.

Genetics ◽  
1999 ◽  
Vol 151 (4) ◽  
pp. 1517-1529 ◽  
Author(s):  
James M Burnette ◽  
Allyson R Hatton ◽  
A Javier Lopez

Abstract Alternatively spliced Ultrabithorax mRNAs differ by the presence of internal exons mI and mII. Two approaches were used to identify trans-acting factors required for inclusion of these cassette exons. First, mutations in a set of genes implicated in the control of other alternative splicing decisions were tested for dominant effects on the Ubx alternative splicing pattern. To identify additional genes involved in regulation of Ubx splicing, a large collection of deficiencies was tested first for dominant enhancement of the haploinsufficient Ubx haltere phenotype and second for effects on the splicing pattern. Inclusion of the cassette exons in Ubx mRNAs was reduced strongly in heterozygotes for hypomorphic alleles of hrp48, which encodes a member of the hnRNP A/B family and is implicated in control of P-element splicing. Significant reductions of mI and mII inclusion were also observed in heterozygotes for loss-of-function alleles of virilizer, fl(2)d, and crooked neck. The products of virilizer and fl(2)d are also required for Sxl autoregulation at the level of splicing; crooked neck encodes a protein with structural similarities to yeast-splicing factors Prp39p and Prp42p. Deletion of at least five other loci caused significant reductions in the inclusion of mI and/or mII. Possible roles of identified factors are discussed in the context of the resplicing strategy for generation of alternative Ubx mRNAs.


2008 ◽  
Vol 5 (2) ◽  
Author(s):  
Dorothea Emig ◽  
Melissa S. Cline ◽  
Karsten Klein ◽  
Anne Kunert ◽  
Petra Mutzel ◽  
...  

SummaryProteins and their interactions are essential for the functioning of all organisms and for understanding biological processes. Alternative splicing is an important molecular mechanism for increasing the protein diversity in eukaryotic cells. Splicing events that alter the protein structure and the domain composition can be responsible for the regulation of protein interactions and the functional diversity of different tissues. Discovering the occurrence of splicing events and studying protein isoforms have become feasible using Affymetrix Exon Arrays. Therefore, we have developed the versatile Cytoscape plugin DomainGraph that allows for the visual analysis of protein domain interaction networks and their integration with exon expression data. Protein domains affected by alternative splicing are highlighted and splicing patterns can be compared.


2017 ◽  
Author(s):  
Amy J. Osborne ◽  
Peter K. Dearden

AbstractThe Developmental Origins of Health and Disease (DOHaD) hypothesis predicts that early-life environmental exposures can be detrimental to later-life health, and that mismatch between the pre- and postnatal environment may contribute to the growing non-communicable disease (NCD) epidemic. Within this is an increasingly recognised role for epigenetic mechanisms; epigenetic modifications can be influenced by, e.g., nutrition, and can alter gene expression in mothers and offspring. Currently, there are no whole-genome transcriptional studies of response to nutritional alteration. Thus, we sought to explore how nutrition affects the expression of genes involved in epigenetic processes in Drosophila melanogaster. We manipulated Drosophila food macronutrient composition at the F0 generation, mismatched F1 offspring back to a standard diet, and analysed the transcriptome of the F0 – F3 generations by RNA-sequencing. At F0, the altered (high protein, low carbohydrate, HPLC) diet increased expression of genes involved in epigenetic processes, with coordinated downregulation of genes involved in immunity, neurotransmission and neurodevelopment, oxidative stress and metabolism. Upon reversion to standard nutrition, mismatched F1 and F2 generations displayed multigenerational inheritance of altered gene expression. By the F3 generation, gene expression had reverted to F0 (matched) levels. These nutritionally-induced gene expression changes demonstrate that dietary alteration can upregulate epigenetic genes, which may influence the expression of genes with broad biological functions. Further, the multigenerational inheritance of the gene expression changes in F1 and F2 mismatched generations suggests a predictive adaptive response (PAR) to maternal nutrition. Our findings may help to understand the interaction between maternal diet and future offspring health, and have direct implications for the current NCD epidemic.


2003 ◽  
Vol 81 (1) ◽  
pp. 25-32 ◽  
Author(s):  
BRIGITTE MORETEAU ◽  
PATRICIA GIBERT ◽  
JEAN-MARIE DELPUECH ◽  
GEORGES PETAVY ◽  
JEAN R. DAVID

1993 ◽  
Vol 12 (5) ◽  
pp. 1853-1870 ◽  
Author(s):  
A.J. Roebroek ◽  
J.W. Creemers ◽  
I.G. Pauli ◽  
T. Bogaert ◽  
W.J. Van de Ven

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