Scientists pinpoint driver of IBD and other disorders with work under way to adapt existing drugs to treat patients
  • threelonmusketeers@sh.itjust.worksEnglish
    6·
    7 months ago

    Lee’s research team “stumbled” on the discovery after investigating a “gene desert”, a stretch of DNA on chromosome 21 that does not code for proteins, which has previously been linked to IBD and other autoimmune diseases. Writing in Nature, they describe how they found a section of DNA that behaves like a volume control for nearby genes. This “enhancer” was seen only in immune cells called macrophages where it boosted a gene called ETS2 and ramped up the risk of IBD.

    Sounds like more “junk” non-coding DNA turns out to be not junk after all. I wonder how much of our DNA is actually junk, and how much we just don’t know yet.

    • phdepressed@sh.itjust.worksEnglish
      9·
      7 months ago

      Modern scientific consensus is largely that “junk” DNA isn’t a thing. All of our DNA has purpose including and sometimes especially the non-coding(nc) parts. The ncRNAs made from ncDNA come in various flavors and are very important to a lot of gene expression control. As seen here that’s ETS2 but pretty much all known genes have ncRNA that affects expression in one way or another.

      Biology at a research level has basically had to throw out the DNA->RNA->protein dogma because they all affect each other and themselves.

      • CanadaPlus@lemmy.sdf.orgEnglish
        2·
        7 months ago

        Well, there’s things like “jumping genes” that don’t necessarily provide anything for the organism, but that’s a bit of a nitpick, since they’re not just random codons, and some do or at least could.