Sexual reproduction provides a unique opportunity for pairwise interactions between genotypes of mating pairs. When male x female interactions are involved, evolution may fail to optimize functions for either sex, and retains a high level of variation. This appears to be the case for factors influencing sperm competition and other reproductive fitness attributes in Drosophila. The accessory gland proteins (Acps) mediate aspects of these interactions, and along with the female molecules that interact with Acps, they will provide a molecular path to quantifying specific male x female interactions. Drosophila sperm competition provides a unique system for studying male x female interactions in sexaul reproduction.
The first aim i s to use genetic isolates from natural populations to quantify male x female interactions in components of sperm competition and ultimately, reproductive fitness with a focus on those likely to be mediated by Acps and the processes that interact in females. Paternity success in doubly mated females, fecundity, fertility, and female receptivity will be scored. This study will quantify reproductive fitness components for validation of the findings of Aim 2.
The second aim i s to dissect male x female interactions by testing RNAi knockdowns of specific male Acp genes across a range of well-characterized wild female genotypes. Comparisons of reproductive phenotypes will be made between control males and males with specific Acps knocked down by RNAi. Focus will be Acps that effect sperm storage or sperm competition. Female lines that are hyper- and hypo-responsive to each knockdown will be identified, and interactions will be partitioned into components mediated by each Acp.
Aim 2 will identify specific interactions of Acps with female backgrounds and female response genes with male backgrounds. This will extend the understanding of the genetic variation in male and female contributions to reproduction, as well as how and why genetic variation is maintained in nature. Since the genes to be examined involve basic reproductive functions, these results will expand the foundation for understanding cases of idiopathic human infertility, specifically those in which no sex-specific cause can be identified and may reflect genetic incompatibility between the partners.

Public Health Relevance

Drosophila melanogaster will be used as a model to quantify the male x female genetic interactions in aspects of fertility. The project aims to understand cases of aberrant fertility of particular genotype-pairs in crosses, when neither genotype by itself is unusual in its fertility. It will also be relevant to explaining the basis for human infertilities that arise from a reproductive incompatibility between the particular pair of individuals involved.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32GM093663-01
Application #
7912462
Study Section
Special Emphasis Panel (ZRG1-F05-C (20))
Program Officer
Bender, Michael T
Project Start
2010-09-30
Project End
2012-09-29
Budget Start
2010-09-30
Budget End
2011-09-29
Support Year
1
Fiscal Year
2010
Total Cost
$47,606
Indirect Cost
Name
Cornell University
Department
Biochemistry
Type
Schools of Earth Sciences/Natur
DUNS #
872612445
City
Ithaca
State
NY
Country
United States
Zip Code
14850
Chow, Clement Y; Avila, Frank W; Clark, Andrew G et al. (2015) Induction of excessive endoplasmic reticulum stress in the Drosophila male accessory gland results in infertility. PLoS One 10:e0119386
Chow, Clement Y; Wang, Xu; Riccardi, David et al. (2015) The genetic architecture of the genome-wide transcriptional response to ER stress in the mouse. PLoS Genet 11:e1004924
Chow, Clement Y; Wolfner, Mariana F; Clark, Andrew G (2013) Using natural variation in Drosophila to discover previously unknown endoplasmic reticulum stress genes. Proc Natl Acad Sci U S A 110:9013-8
Chow, Clement Y; Wolfner, Mariana F; Clark, Andrew G (2013) Large neurological component to genetic differences underlying biased sperm use in Drosophila. Genetics 193:177-85