Discernible phenotypic alterations following linc-10 knockout in Caenorhabditis elegans
Long noncoding RNAs (lncRNAs) are regulatory molecules that play vital roles in various cellular processes. Although the loss of function of most annotated lncRNAs in several model organisms does not result in severe phenotypes, suggesting they are not essential for survival or reproduction, lncRNAs may still act as responsive elements under diverse physiological and pathological conditions. In this study, we investigated the role of the linc-10 gene in Caenorhabditis elegans and found that it regulates gene expression and contributes to normal fertility. Knockout (KO) mutants of linc-10 exhibited mild but notable abnormalities, including reduced brood size, altered developmental trajectories, and increased sensitivity to stress, along with occasional sterility and a slightly elevated male ratio. We characterized the expression patterns of linc-10 across developmental stages and performed high-throughput sequencing to detect differentially expressed genes (DEGs) following linc-10 deletion. We found that several immune-related genes were dysregulated. Notably, linc-10 mutants showed increased susceptibility to Pseudomonas aeruginosa PA14 infection and other stressors. Moreover, piRNA levels were altered, and the expression of the Piwi/PRG-1 Argonaute protein was reduced in KO animals, suggesting that linc-10 may regulate gene expression through piRNA pathways. In conclusion, our findings highlight a potential role for animal lncRNAs in maintaining physiological reproductive and immune functions.
Authors
- Xiao‐Man Sun (ORCID: https://orcid.org/0000-0002-6268-4546)
- Rongrong Wu (ORCID: https://orcid.org/0000-0003-3876-1609)
- He Chen (ORCID: https://orcid.org/0009-0002-4611-9974)
Institutions
- Anhui University (CN)
Publication Details
- Journal
- Non-coding RNA Research
- Published
- 2026-11-04
- DOI
- https://doi.org/10.1016/j.ncrna.2026.10.004
- Primary Topic
- Cancer-related molecular mechanisms research
- Type
- article
- Field-Weighted Citation Impact
- 0.00