Journal article
Intracellular signaling in proto-eukaryotes evolves to alleviate regulatory conflicts of endosymbiosis
- Abstract:
- The complex eukaryotic cell resulted from a merger between simpler prokaryotic cells, yet the role of the mitochondrial endosymbiosis with respect to other eukaryotic innovations has remained under dispute. To investigate how the regulatory challenges associated with the endosymbiotic state impacted genome and network evolution during eukaryogenesis, we study a constructive computational model where two simple cells are forced into an obligate endosymbiosis. Across multiple in silico evolutionary replicates, we observe the emergence of different mechanisms for the coordination of host and symbiont cell cycles, stabilizing the endosymbiotic relationship. In most cases, coordination is implicit, without signaling between host and symbiont. Signaling only evolves when there is leakage of regulatory products between host and symbiont. In the fittest evolutionary replicate, the host has taken full control of the symbiont cell cycle through signaling, mimicking the regulatory dominance of the nucleus over the mitochondrion that evolved during eukaryogenesis
- Publication status:
- Published
- Peer review status:
- Peer reviewed
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(Preview, Version of record, pdf, 2.9MB, Terms of use)
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- Publisher copy:
- 10.1371/journal.pcbi.1011860
- Publication website:
- https://dspace.library.uu.nl/bitstream/1874/438402/1/journal.pcbi.1011860.pdf
Authors
+ Nederlandse Organisatie voor Wetenschappelijk Onderzoek
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- Funder identifier:
- 10.13039/501100003246
- Grant:
- 016.160.638
- Publisher:
- Public Library of Science
- Journal:
- PLoS Computational Biology More from this journal
- Volume:
- 20
- Issue:
- 2
- Pages:
- e1011860-e1011860
- Publication date:
- 2024-02-09
- DOI:
- EISSN:
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1553-7358
- ISSN:
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1553-734X
- Language:
-
English
- Keywords:
- Pubs id:
-
1676263
- Local pid:
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pubs:1676263
- Source identifiers:
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W4391677517
- Deposit date:
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2026-06-08
- ARK identifier:
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Terms of use
- Copyright date:
- 2024
- Licence:
- CC Attribution (CC BY)
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