The long-term objective of our research is to investigate the patterns that arise as a result of gene duplication to better understand the evolutionary forces that drive genome architecture. Meiotic sex chromosome inactivation (MSCI), the level of gene expression and sexual antagonism have been proposed to explain the patterns of duplication of male-biased genes in flies. However, MSCI or the level of expression cannot account for several observations, including the abundance of autosome-to-autosome duplicates;the observation that certain genes are duplicated while others are not even though all X-linked housekeeping genes should be under strong selective pressure to duplicate;the continued occurrence of gene duplications or the recurrence of duplications of some genes in the same lineage;or the loss of duplicated genes that evolved under positive selection. Additionally, most models of sexual antagonism do not incorporate gene duplication and instead propose that the dominance of the mutations can explain the location of sex-biased genes. Models that incorporate gene duplication do not consider that the sexually antagonistic selection begins with the parental gene (i.e., for parental alleles) and in autosomes and that it will continue after heteromorphic sex chromosomes and MSCI have evolved. An innovative model based on our results from the previous funding period is introduced in which gene duplication is considered to be an important mechanism to generate male germline functions and is proposed to resolve intralocus sexually antagonistic conflicts for housekeeping genes (i.e., selection operating already on the parental gene) driven by tissue antagonism (i.e., testis antagonism). It is now clear that the testes are subject to strong selection due to male competition, segregation distortion and/or parasite-related conflicts, and this is driving rapid evolution at the protein level and likely in regulatory regions. Under this model, gene turnover is also expected to be high. This project has three aims to study the function and antagonistic effects of new genes and parental genes as well as the evolutionary rate and structure of testes-specific regulatory regions.
Aim 1 focuses on the function and role of testes-specific nuclear transport genes and their parental genes with respect to male germline conflicts.
Aim 2 will investigate the antagonistic effects of a subset of the new testes-specific genes and parental nuclearly encoded mitochondrial gene variations.
Aim 3 addresses the study of the rate of evolution of testes-specific regulatory regions and their potential bidirectional nature. Knockouts, knockdowns and tagged proteins will be used to study effects, interactions, cellular localization and co-expression of the genes. New genes or variants of parental genes will be expressed ectopically and the effects on fertility and lifespan will be studied. Whole genome polymorphism data from D. melanogaster and comparative genomics will be exploited using the most current bioinformatics tools and molecular evolution software to achieve these objectives.

Public Health Relevance

In this proposal, we provide an original perspective on topics under intense study, such as patterns of gene duplication, sex-biased expression and the genomic location of sexually antagonistic traits and sexually dimorphic traits. We propose a novel hypothesis describing a new, overlooked role for gene duplication in the resolution of the intralocus sexually antagonistic conflict. The conceptual framework of current thinking on this topic will change if our thesis is supported, as this will imply that new sex-biased duplicate genes are often created from antagonistic alleles of housekeeping genes to resolve sexual antagonism driven by specialization and conflicts in sex-specific tissues.

National Institute of Health (NIH)
National Institute of General Medical Sciences (NIGMS)
Research Project (R01)
Project #
Application #
Study Section
Genetic Variation and Evolution Study Section (GVE)
Program Officer
Eckstrand, Irene A
Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
University of Texas Arlington
Schools of Arts and Sciences
United States
Zip Code
Sorourian, Mehran; Kunte, Mansi M; Domingues, Susana et al. (2014) Relocation facilitates the acquisition of short cis-regulatory regions that drive the expression of retrogenes during spermatogenesis in Drosophila. Mol Biol Evol 31:2170-80
Gallach, Miguel; Betran, Esther (2011) Intralocus sexual conflict resolved through gene duplication. Trends Ecol Evol 26:222-8
Hosken, David J (2011) Gene duplication might not resolve intralocus sexual conflict. Trends Ecol Evol 26:556-7; author reply 558-9
Tracy, Charles; Rio, Javier; Motiwale, Mansi et al. (2010) Convergently recruited nuclear transport retrogenes are male biased in expression and evolving under positive selection in Drosophila. Genetics 184:1067-76
Quezada-Diaz, Jorge Ernesto; Muliyil, Taniya; Rio, Javier et al. (2010) Drcd-1 related: a positively selected spermatogenesis retrogene in Drosophila. Genetica 138:925-37
Sorourian, Mehran; Betran, Esther (2010) Turnover and lineage-specific broadening of the transcription start site in a testis-specific retrogene. Fly (Austin) 4:3-11
Bai, Yongsheng; Casola, Claudio; Betran, Esther (2009) Quality of regulatory elements in Drosophila retrogenes. Genomics 93:83-9
Bai, Yongsheng; Casola, Claudio; Betran, Esther (2008) Evolutionary origin of regulatory regions of retrogenes in Drosophila. BMC Genomics 9:241
Bai, Yongsheng; Casola, Claudio; Feschotte, Cedric et al. (2007) Comparative genomics reveals a constant rate of origination and convergent acquisition of functional retrogenes in Drosophila. Genome Biol 8:R11
Casola, Claudio; Lawing, A Michelle; Betran, Esther et al. (2007) PIF-like transposons are common in drosophila and have been repeatedly domesticated to generate new host genes. Mol Biol Evol 24:1872-88

Showing the most recent 10 out of 11 publications