https://english.elpais.com/science-tech/2025-03-05/new-inheritance-mechanism-unrelated-to-dna-is-discovered-by-chance.htmlQuote
Matthew Eroglu and his research group at the University of Toronto were beginning to study cancer signalling pathways when something strange happened that turned the whole focus of the research on its head. The worms they were using, normally hermaphrodites that reproduce without difficulty, began to become more feminine with each generation until they ended up being sterile.
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yet had nothing to do with any nucleic acid (DNA or RNA) or anything related to them, representing a break with what was known until then about animals. That something — and this was the final surprise — turned out to be proteins with an amyloid structure and prion properties, similar to those that accumulate in Alzheimer’s plaques, which could be passed from generation to generation and multiply over time, vampirizing their neighbors.
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Amyloid proteins can be very different, but they are named after a certain structure they form when they fold. And they have a very peculiar characteristic: they have the potential to multiply by “infecting” other similar proteins with which they come into contact. This “vampirization” is the way prions, which are essentially another type of amyloid protein, spread. Although their reputation is terrifying, their characteristics also allow them to play important roles, such as in the storage of hormones or possibly also in the formation of memory. And, as Harvard University professor Craig P. Hunter writes in a text about the new discovery: “In the same way as DNA, amyloids replicate themselves using themselves as a model, which makes them ideal carriers of acquired, inheritable information.” This, which had been seen in yeast, is now being confirmed for the first time in much more complex animals.
This is huge
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Eroglu admits that it is not known what could cause the accumulation of these proteins or whether they play a role in us, but he also points out that “amyloid aggregates have been observed in human oocytes, although we do not know what they do or what their relevance might be,” and that “at least one group is investigating whether this amyloid inheritance occurs in rats.” This group is led by Gail Cornwall, a researcher at the University of Texas. Asked about this work and its implications, she says that she was “excited.” Amyloid proteins “are an ideal mechanism for organisms to try out new phenotypes [observable traits] before genetically modifying them. One might think that nature would not eliminate such a powerful adaptation mechanism in higher organisms,”
Time to find out.
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“The major implication of this is that stably heritable proteins may act as a reservoir of yet unexplored phenotypic modifiers that are independent of gene sequence, a potential source of ‘missing’ heritability. Though speculative, the breadth of familial traits associated with amyloid perturbations that largely cannot be attributed to genomic sequence variation (for example, type 2 diabetes, some cancers, Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and the autism spectrum) is suggestive of this notion.”