Asexual reproduction reduces transposable element load in experimental yeast populations
Theory predicts that sexual reproduction can either facilitate or restrain transposable element (TE) accumulation by providing TEs with a means of spreading to all individuals in a population, versus facilitating TE load reduction via purifying selection. By quantifying genomic TE loads over time in experimental sexual and asexual Saccharomyces cerevisiae populations, we provide direct evidence that TE loads decrease rapidly under asexual reproduction.. We show, using simulations, that this reduction may occus via evolution of TE activity, most likely via increased excision rates. Thus, sex is a major driver of genomic TE loads and at the root of the success of TEs.
Raw read data of the experiment is available at SRA (BioProject identifier PRJNA308843). All data processing and analyses scripts as well as the simulator together with explanations are available at https://github.com/KamilSJaron/reproductive_mode_TE_dynamics.
Sex speeds adaptation by altering the dynamics of molecular evolutionNCBI BioProject, PRJNA308843.
Article and author information
Deutsche Forschungsgemeinschaft (BA 5800/1-1)
- Jens Bast
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (PP00P3_17062)
- Tanja Schwander
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (PP00P3_139013)
- Tanja Schwander
Deutsche Forschungsgemeinschaft (BA 5800/2-1)
- Jens Bast
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
- Graham Coop, University of California, Davis, United States
- Received: May 17, 2019
- Accepted: September 4, 2019
- Accepted Manuscript published: September 5, 2019 (version 1)
- Version of Record published: October 8, 2019 (version 2)
© 2019, Bast et al.
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.
- Page views
Article citation count generated by polling the highest count across the following sources: Scopus, Crossref, PubMed Central.
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
- Evolutionary Biology
Spider venoms are a complex concoction of enzymes, polyamines, inorganic salts, and disulfide-rich peptides (DRPs). Although DRPs are widely distributed and abundant, their bevolutionary origin has remained elusive. This knowledge gap stems from the extensive molecular divergence of DRPs and a lack of sequence and structural data from diverse lineages. By evaluating DRPs under a comprehensive phylogenetic, structural and evolutionary framework, we have not only identified 78 novel spider toxin superfamilies but also provided the first evidence for their common origin. We trace the origin of these toxin superfamilies to a primordial knot – which we name ‘Adi Shakti’, after the creator of the Universe according to Hindu mythology – 375 MYA in the common ancestor of Araneomorphae and Mygalomorphae. As the lineages under evaluation constitute nearly 60% of extant spiders, our findings provide fascinating insights into the early evolution and diversification of the spider venom arsenal. Reliance on a single molecular toxin scaffold by nearly all spiders is in complete contrast to most other venomous animals that have recruited into their venoms diverse toxins with independent origins. By comparatively evaluating the molecular evolutionary histories of araneomorph and mygalomorph spider venom toxins, we highlight their contrasting evolutionary diversification rates. Our results also suggest that venom deployment (e.g. prey capture or self-defense) influences evolutionary diversification of DRP toxin superfamilies.
- Evolutionary Biology
- Microbiology and Infectious Disease
Increasing numbers of small proteins with diverse physiological roles are being identified and characterized in both prokaryotic and eukaryotic systems, but the origins and evolution of these proteins remain unclear. Recent genomic sequence analyses in several organisms suggest that new functions encoded by small open reading frames (sORFs) may emerge de novo from noncoding sequences. However, experimental data demonstrating if and how randomly generated sORFs can confer beneficial effects to cells are limited. Here we show that by up-regulating hisB expression, de novo small proteins (≤ 50 amino acids in length) selected from random sequence libraries can rescue Escherichia coli cells that lack the conditionally essential SerB enzyme. The recovered small proteins are hydrophobic and confer their rescue effect by binding to the 5' end regulatory region of the his operon mRNA, suggesting that protein binding promotes structural rearrangements of the RNA that allow increased hisB expression. This study adds RNA regulatory elements as another interacting partner for de novo proteins isolated from random sequence libraries, and provides further experimental evidence that small proteins with selective benefits can originate from the expression of nonfunctional sequences.