Happy Halloween from the Green Center! Awesome pumpkin carving by @purbita_s31 🎃
Look who earned an unconditional pass on her qualifying exam today! Congratulations to Purbita Saha! @GDDgradprogUTSW @UTSWGradSchool @UTSWScience #ProudPI 🤩
We have another PhD candidate in the Bana Lab! Congratulations to Ryan for all the creativity and hard work that went into his proposal - well deserved! Here's Ryan enjoying a pre-covid coffee with @aishwaryagogate and @SaraMartire 😊.
Say hello to the newest PhD candidate from the Bana lab! Huge congrats to @sdharx and well-deserved! Watch out, she means business 😳
Interested in starting your own lab studying mechanisms of gene regulation? Come join us at UTSW in the incredibly supportive Green Center!
Amanuel @amanuel_MT in action at his #moet2019 poster tonight. Awesome job!! He’s here all week, folks.
Finally, thank you to DISD for ending the school year just in time for me to be here when the paper came out last Friday.
The problem comes when we ask cells to change their transcription program. In this case, we find that the H3.3 KO cells can't effectively activate enhancers during differentiation.
Since the H3.3 KO ESCs lose ~50% of H3K27ac, we thought we might observe global effects on transcription. The third surprise - H3.3 KO ESCs can tolerate reduced H3K27ac and do not experience global reductions in transcription.
We expected that this would be a phos/ac cis crosstalk. The second surprise - H3.3S31ph stimulates p300 activity on *other* nucleosomes in a trans mechanism.
We looked at differences in the H3.3 sequence compared to canonical H3. The only difference in the tails is at position 31 - H3.3S31 (a phosphorylation site!) vs H3A31. Addback experiments show that H3.3S31 is needed to restore H3K27ac in the H3.3 KO cells.
The first surprise - this happens without changing the "open" state of these regions or the level of p300 recruitment. So, something about H3.3 stimulates p300 activity.





















