Transgenerational Inheritance of an Acquired Small RNA-Based Antiviral Response in C. elegans
Open accessAbstract
Induced expression of the Flock House virus in the soma of C. elegans results in the RNAi-dependent production of virus-derived, small-interfering RNAs (viRNAs), which in turn silence the viral genome. We show here that the viRNA-mediated viral silencing effect is transmitted in a non-Mendelian manner to many ensuing generations. We show that the viral silencing agents, viRNAs, are transgenerationally transmitted in a template-independent manner and work in trans to silence viral genomes present in animals that are deficient in producing their own viRNAs. These results provide evidence for the transgenerational inheritance of an acquired trait, induced by the exposure of animals to a specific, biologically relevant physiological challenge. The ability to inherit such extragenic information may provide adaptive benefits to an animal.
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There is no evidence for the modification of the genetic core (DNA sequence) based on acquired characteristics.
“The ‘inheritance of acquired characteristics’ has been suggested, although few mechanisms have been proposed, and there is no evidence for the modification of the genetic core (DNA sequence) based on acquired characteristics [157,159].”
From Opinion: The Key Steps in the Origin of Life to the Formation of the Eukaryotic Cell (2024) · cites this paper as [159]
The Introduction and Discussion (pages unavailable in our copy) support inheritance of an acquired antiviral response through small RNAs rather than a genetic template. They do not establish the broader claim that there is no evidence for acquired characteristics modifying DNA sequence. (LLM, conf=0.83)
Experimental — accuracy not yet measuredShort RNAs produced by hunger and viral infection cause inheritance.
“In contrast, short RNAs produced by hunger and viral infection cause inheritance [100,101,102].”
From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [100]
The Discussion (page not available) says that small viRNAs induced by viral replication pass through the germline across generations, supporting the viral-infection part of the claim. Our copy does not report hunger-induced small RNAs or inheritance caused by hunger, so it does not support that part. (LLM, conf=0.88)
Experimental — accuracy not yet measuredC. elegans can translate a variety of environmental inputs, including viral infection, famine, and high temperatures, into modifications of some epigenetic elements.
“With a different model, it has been demonstrated that C. elegans can translate a variety of environmental inputs, including viral infection, famine, and high temperatures, into modifications of some epigenetic elements.”
From Revisiting Epigenetics Fundamentals and Its Biomedical Implications (2024) · cites this paper as [100]
The Introduction and Discussion describe an antiviral response in C. elegans that is carried across generations by virus-derived small RNAs. The paper does not establish famine or high temperatures as environmental triggers of epigenetic changes; its heat shock is used to induce expression of a viral transgene. The claim therefore extends the paper’s finding beyond the input it studied. (LLM, conf=0.88)
Experimental — accuracy not yet measuredC. elegans converts several environmental stimuli, including viral infection, starvation and elevated temperature, into changes in epigenetic components.
“C. elegans has been shown to translate several environmental stimuli, such as viral infection, starvation or elevated temperatures, into modification of epigenetic components [77][78][79] .”
From Advances in epigenetics link genetics to the environment and disease (2019) · cites this paper as [77]
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- Authors
- Rechavi, O., Minevich, G., & Hobert, O.
- Affiliations
- Howard Hughes Medical Institute (US)
- Corresponding author
- Rechavi, Oded
- Hobert, Oliver
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2011-12
- Volume
- 147
- Issue
- 6
- Pages
- 1248-1256
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3250924
- OpenAlex
- W2001603328
- Cited by
- 351
- References
- 38
- Citations by year
- 2026: 6 · 2025: 14 · 2024: 25 · 2023: 27 · 2022: 22 · 2021: 26 · 2020: 24 · 2019: 23 · 2018: 24 · 2017: 28 · 2016: 26 · 2015: 17 · 2014: 26 · 2013: 35 · 2012: 24
- FWCI
- 11.16
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 630 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (T32HD055165)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Interference and Gene Delivery
- Life Sciences › Immunology and Microbiology › Immunology › Invertebrate Immune Response Mechanisms
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Chromosomal and Genetic Variations
- Keywords
- transgenerational inheritance, adaptive immunity, siRNA, Flock House virus, RNA interference, Caenorhabditis elegans, non-Mendelian inheritance, antiviral response
- MeSH terms
- Animals, Extrachromosomal Inheritance, RNA, Viral, Genome, Viral, Caenorhabditis elegans, Nodaviridae, RNA Interference, RNA, Small Interfering
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