Self-sperm induce resistance to the detrimental effects of sexual encounters with males in hermaphroditic nematodes

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Abstract

Sexual interactions have a potent influence on health in several species, including mammals. Previous work in C. elegans identified strategies used by males to accelerate the demise of the opposite sex (hermaphrodites). But whether hermaphrodites evolved counter-strategies against males remains unknown. Here we discover that young C. elegans hermaphrodites are remarkably resistant to brief sexual encounters with males, whereas older hermaphrodites succumb prematurely. Surprisingly, it is not their youthfulness that protects young hermaphrodites, but the fact that they have self-sperm. The beneficial effect of self-sperm is mediated by a sperm-sensing pathway acting on the soma rather than by fertilization. Activation of this pathway in females triggers protection from the negative impact of males. Interestingly, the role of self-sperm in protecting against the detrimental effects of males evolved independently in hermaphroditic nematodes. Endogenous strategies to delay the negative effect of mating may represent a key evolutionary innovation to maximize reproductive success.

Data availability

Sequencing data have been deposited in NCBI SRA under accession code PRJNA508378

The following data sets were generated

1. Booth LN
2. Maures TJ
3. Yeo RW
4. Brunet A
(2019) Transcriptomic profiling of C. elegans hermaphrodites and feminized (fem-1) individuals following a 2 hour interaction with males or without a male interaction
NCBI Sequence Read Archive, PRJNA508378.

http://www.ncbi.nlm.nih.gov/bioproject/?term=PRJNA508378

Article and author information

Author details

Lauren N Booth

Department of Genetics, Stanford University, Stanford, United States

Competing interests
No competing interests declared.
Travis J Maures

Department of Genetics, Stanford University, Stanford, United States

Competing interests
Travis J Maures, is affiliated with Synthego. The author has no financial interests to declare..
Robin W Yeo

Department of Genetics, Stanford University, Stanford, United States

Competing interests
No competing interests declared.
Cindy Tantilert

Department of Genetics, Stanford University, Stanford, United States

Competing interests
No competing interests declared.
Anne Brunet

Department of Genetics, Stanford University, Stanford, United States

For correspondence
abrunet1@stanford.edu

Competing interests
No competing interests declared.

"This ORCID iD identifies the author of this article:" 0000-0002-4608-6845

Funding

National Institutes of Health (DP1 AG044848)

Anne Brunet

National Institutes of Health (R01 AG054201)

Anne Brunet

Helen Hay Whitney Foundation (Joan Whitney Payson Scholar)

Lauren N Booth

National Institutes of Health (K99 AG051738)

Lauren N Booth

Genentech Foundation (Genentech Foundation Predoctoral Fellow)

Robin W Yeo

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Copyright

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.