David Bartel's Lab
David Bartel's lab @WhiteheadInst @MIT @HHMI | microRNAs, mRNAs, and other RNAs
- Reposted by David Bartel's LabDoes the noncoding genome actually carry more genetic information than coding seqs? Motivated by this question we mutated every bp in the 10kb MYC locus. Results are even more exciting: Decoding the MYC locus reveals a druggable ultraconserved RNA element www.biorxiv.org/content/10.6...
- We’re excited to share our latest preprint on the mechanism of excised linear intron stabilization in yeast! This work was led by PhD student @glennli.bsky.social and was a wonderful collaboration with @maxewilkinson.bsky.social. Link: www.biorxiv.org/content/10.6... (1/4)
- In budding yeast cultured under saturation or other prolonged stresses, ~10% of introns accumulate post-splicing as stable, linear RNAs that are protected by the spliceosome. We set out to understand how these stable introns remain associated with the spliceosome and escape canonical RNA decay.(2/4)
- In the process of solving this mystery, we discovered a new, atypical conformation of the spliceosome and discovered that the spliceosome has a surprising propensity to reassemble on excised linear introns in both stressed and unstressed conditions. (3/4)
- Huge thanks to @maxewilkinson.bsky.social for making this work possible! (4/4)
- Reposted by David Bartel's LabFirst preprint of the year! New work from @jimmy-ly.bsky.social revealing unexpected roles for 5' UTR length in controlling alternate translational isoforms - important implications for both physiological cell function and rare disease. Small changes -> big impacts. www.biorxiv.org/content/10.6...
- Reposted by David Bartel's LabWe are looking for a postdoc to work on mechanisms of #RNA decay in cancer using #cryoEM with #nanobodies and #minibinders! Please RT
- Check our latest collaboration with the Kleaveland Lab (kleavelandlab.org), led by Joanna Stefano and Lara Elcavage: academic.oup.com/nar/article/... (1/2)
- We find that disrupting the miR-200–ZEB1 double-negative feedback loop leads to anovulatory infertility and widespread gene expression changes in the mouse pituitary. This study demonstrates the dramatic phenotypic and molecular consequences of disrupting repression of a single miRNA target. (2/2)
- We are thrilled to share our latest work uncovering the mechanistic basis of target-directed microRNA degradation (TDMD). This work was driven by @jakobfarnung.bsky.social and @elenaslo.bsky.social in a fantastic collaboration with Brenda Schulman's lab. tinyurl.com/E3TDMD (1/5)
- The ZSWIM8 E3 ligase was known to cause degradation of AGO–microRNA complexes bound to trigger RNAs. However, whether and how ZSWIM8 directly recognizes these complexes among the preponderance of non-trigger-bound AGO–microRNA complexes in the cell has been a mystery. (2/5)
- We demonstrate selective binding of ZSWIM8 to a human AGO–microRNA–trigger complex for CUL3-mediated polyubiquitylation of the AGO protein. Furthermore, cryo-EM analyses reveal how ZSWIM8 recognizes the distinct AGO and RNA conformations shaped by pairing of the microRNA to the trigger. (3/5)
-
View full threadHuge thanks to Brenda Schulman and @jakobfarnung.bsky.social for the exceptionally collaborative effort from start to finish. We also thank @wyppeter.bsky.social, Lianne Blodgett, and Daniel Lin for their invaluable contributions to this work! (5/5)
- Reposted by David Bartel's LabFrom an accidental discovery of hidden biology to a new framework to understanding and diagnosing rare disease. Thrilled to share the most recent work from our lab and the amazing Jimmy Ly. wi.mit.edu/news/alterna...
- Check out the latest work from our lab, led by Daniel Lin and Lara Elcavage: www.biorxiv.org/content/10.1... (1/3)
- We identify 5 sites in 3' UTRs of mRNAs that trigger target-directed microRNA degradation (TDMD) of miR-335-3p, miR-322, and miR-503, uncovering noncoding functions of these mRNAs. This study positions TDMD within imprinted gene networks on the battleground of parental conflict (2/3)
- Check out related work by the Mendell lab (@mendell-lab.bsky.social) and the Xie lab: www.biorxiv.org/content/10.1..., www.biorxiv.org/content/10.1... (3/3)
- Check out the latest work from our lab, led by Arash Latifkar @ara-latifkar.bsky.social , www.biorxiv.org/content/10.1...
- We've uncovered two mechanisms that coronaviruses use to solve the “tailomere problem” and identified an mRNA degradation pathway that operates independently of viral protein nsp1. Many thanks to Eugene Valkov's lab (@eugenevalkov.bsky.social) for their help with this study.
- Check out the latest work from Jordan Ray (@jordanray.bsky.social), a collaboration between our lab and David Sabatini’s lab. www.biorxiv.org/content/10.1... (1/2)
- Since their discovery, we have known lysosomes possess RNase activity; however, their endogenous substrates were not known. Surprisingly we found preferential targeting of specific RNAs for lysosomal degradation by autophagy and identified sequence motifs that mediate their lysosomal targeting (2/2)
- Reposted by David Bartel's Lab[Not loaded yet]
- Check out the latest study from our lab, led by Coffee Xiang (@coffeebond007.bsky.social) www.nature.com/articles/s41... (1/2)
- We developed a neural network machine-learning model that predicts poly(A) tail-length changes in frog, mouse, and human oocytes, revealing new regulatory motifs and showing that variants disrupting tail lengthening are under negative selection, thus linking tail-length control to human fertility.
- Reposted by David Bartel's LabNew preprint! We solve a mystery you didn't know existed. Mitotic cells lack new transcription but require ongoing translation. Interphase mRNA half life is only 2-4 hrs. So how do cells arrest in mitosis for hours without depleting their transcriptomes? www.biorxiv.org/content/10.1...
- Don’t miss this Q&A with Dr. Michelle Frank (@michelle-frank.bsky.social), an awesome postdoc in our lab!
- Check out the latest study from our lab, led by @mhall98.bsky.social : www.biorxiv.org/content/10.1... (1/2)
- We report that some miRNAs are capable of high affinity binding to 3′-only sites (stretches of extensive perfect pairing to the 3′ region, without any pairing to the miRNA seed) and that these sites are functional, imparting post-transcriptional repression to site-containing reporter mRNAs. (2/2)
- Reposted by David Bartel's Lab[Not loaded yet]
