@vishal-d-patel.bsky.social
Physician-Scientist l Professor I Nephrologist l Polycystic Kidney Disease & Genetics l miRNAs, ncRNAs, RNA-therapeutics, Anti-miRs/ASOs l @UTSWNews
It was a pleasure to write this commentary. Thank you for the invite
@jclinical-invest.bsky.social
This work opens up new ideas for:
π§ͺ Kidney regenerative strategy
π‘ Nutrient-epigenetic regulation
𧫠Improving kidney organoids
πΆ Reduced nephron endowment conditions, such as low birth weight & preterm birth
Huge thanks to our collaborators π
#SciComm #KidneyResearch #STEM
π₯ One of our most exciting findings:
Uptitrating this pathway via SAM supplementation or METTL3 pharmaceutical activation facilitates an 'induced' nephron progenitor population and increases nephron production.
Essentially: SAM β RNA methylation β increased nephron endowment
We show using genetic gain and loss-of-function that METTL3 is necessary and sufficient for NPC differentiation and nephrogenesis.
Similarly, methionine and SAM, in a METTL3-dependent manner, are required for NPC differentiation and nephrogenesis.
The key player is METTL3, an mβΆA RNA methyltransferase.
METTL3 senses SAM levels in nephron progenitors and methylates mRNAs like Lrpprc, influencing whether nephron progenitors differentiate or self-renew.
Essentially: Nutrients/Metabolism β Epitranscriptomics β Nephrogenesis. π§©
Thrilled to share our new work in Nature Communications!
We discovered how methionine β SAM β METTL3 β RNA methylation axis guides kidney development, especially nephron progenitor differentiation. #Nephrology #Epitranscriptomics
Hereβs a quick breakdown
www.nature.com/articles/s41...
Texas fall evening....beautiful Lake Grapevine
17.11.2024 23:52 β π 1 π 0 π¬ 0 π 0
