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TitleTFIIH kinase CDK7 drives cell proliferation through a common core transcription factor network.
Journal, issue, pagesSci Adv, Vol. 11, Issue 9, Page eadr9660, Year 2025
Publish dateFeb 28, 2025
AuthorsTaylor Jones / Junjie Feng / Olivia Luyties / Kira Cozzolino / Lynn Sanford / Jenna K Rimel / Christopher C Ebmeier / Grace S Shelby / Lotte P Watts / Jessica Rodino / Nisha Rajagopal / Shanhu Hu / Finn Brennan / Zachary L Maas / Sydney Alnemy / William F Richter / Adrian F Koh / Nora B Cronin / Ameya Madduri / Jhuma Das / Elliot Cooper / Kristin B Hamman / John P Carulli / Mary A Allen / Sabrina Spencer / Abhay Kotecha / Jason J Marineau / Basil J Greber / Robin D Dowell / Dylan J Taatjes /
PubMed AbstractHow cyclin-dependent kinase 7 (CDK7) coordinately regulates the cell cycle and RNA polymerase II transcription remains unclear. Here, high-resolution cryo-electron microscopy revealed how two ...How cyclin-dependent kinase 7 (CDK7) coordinately regulates the cell cycle and RNA polymerase II transcription remains unclear. Here, high-resolution cryo-electron microscopy revealed how two clinically relevant inhibitors block CDK7 function. In cells, CDK7 inhibition rapidly suppressed transcription, but constitutively active genes were disproportionately affected versus stimulus-responsive. Distinct transcription factors (TFs) regulate constitutive versus stimulus-responsive genes. Accordingly, stimulus-responsive TFs were refractory to CDK7 inhibition whereas constitutively active "core" TFs were repressed. Core TFs (n = 78) are predominantly promoter associated and control cell cycle and proliferative gene expression programs across cell types. Mechanistically, rapid suppression of core TF function can occur through CDK7-dependent phosphorylation changes in core TFs and RB1. Moreover, CDK7 inhibition depleted core TF protein levels within hours, consistent with durable target gene suppression. Thus, a major but unappreciated biological function for CDK7 is regulation of a TF cohort that drives proliferation, revealing an apparent universal mechanism by which CDK7 coordinates RNAPII transcription with cell cycle CDK regulation.
External linksSci Adv / PubMed:40020069 / PubMed Central
MethodsEM (single particle)
Resolution2.3 - 2.4 Å
Structure data

19627

8s0r

EMDB-19627, PDB-8s0r:
Cryo-EM structure of CAK modified by covalent inhibitor SY-1365
Method: EM (single particle) / Resolution: 2.4 Å

19628

8s0t

EMDB-19628, PDB-8s0t:
Cryo-EM structure of CAK in complex with SY-5609
Method: EM (single particle) / Resolution: 2.3 Å

Chemicals

PDB-1h46:
The catalytic module of Cel7D from Phanerochaete chrysosporium as a chiral selector: Structural studies of its complex with the b-blocker (R)-propranolol

ChemComp-HOH:
WATER


ChemComp, No image

ChemComp-YNK:
Unknown entry

Source
  • homo sapiens (human)
KeywordsTRANSCRIPTION / Kinase / covalent inhibitor / cell cycle

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