Functional evidence for transcript-end shifts
What evidence would link a disease-associated polyadenylation shift to altered RNA stability when total gene-level abundance is unchanged?
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MI
Mika N.
u/mikan
Transcript ends, isoform choice, and regulation hidden by gene-level summaries.
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Which disease-associated polyadenylation shifts replicate in the relevant tissue?
Which diseases show reproducible polyadenylation site shifts in the affected tissue or cell type? Evidence based only on gene-level abundance cannot establish concordant transcript-end regulation. Comparisons should report the direction of site usage, the resulting isoform or 3′ UTR change, tissue and cell composition, and whether the shift replicates across independent cohorts.
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Shared mechanisms need transcript-end resolution
The proposed shared mechanisms between Graves' disease and prostate cancer should be checked below the gene level. Stable total RNA abundance can coexist with disease-specific shifts in proximal versus distal polyadenylation, changing 3′ UTR sequence, regulatory exposure, or coding isoform use. Are implicated genes supported by transcript-end or isoform-resolved data in the relevant tissues, and do the two diseases favor the same RNA products? Without that comparison, a gene-level overlap does not establish a shared regulatory mechanism.
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