Genes & Development
Papers 8,304
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#1Mengle Shao (UTSW: University of Texas Southwestern Medical Center)H-Index: 25
#2Qianbin Zhang (UTSW: University of Texas Southwestern Medical Center)H-Index: 4
Last. Rana K. Gupta (UTSW: University of Texas Southwestern Medical Center)H-Index: 34
view all 8 authors...
Energy-storing white adipocytes maintain their identity by suppressing the energy-burning thermogenic gene program of brown and beige adipocytes. Here, we reveal that the protein-protein interaction between the transcriptional coregulator ZFP423 and brown fat determination factor EBF2 is essential for restraining the thermogenic phenotype of white adipose tissue (WAT). Disruption of the ZFP423-EBF2 protein interaction through CRISPR-Cas9 gene editing triggers widespread "browning" of WAT in adul...
#1Yuxiao Zhou (SJTU: Shanghai Jiao Tong University)H-Index: 1
#2Siyuan Xu (SJTU: Shanghai Jiao Tong University)
Last. Qiang Wu (SJTU: Shanghai Jiao Tong University)H-Index: 24
view all 4 authors...
Enhancers generate bidirectional noncoding enhancer RNAs (eRNAs) that may regulate gene expression. At present, the eRNA function remains enigmatic. Here, we report a 5' capped antisense eRNA PEARL (Pcdh eRNA associated with R-loop formation) that is transcribed from the protocadherin (Pcdh) α HS5-1 enhancer region. Through loss- and gain-of-function experiments with CRISPR/Cas9 DNA fragment editing, CRISPRi, and CRISPRa, as well as locked nucleic acid strategies, in conjunction with ChIRP, MeDI...
#1Jacob Paiano (NIH: National Institutes of Health)H-Index: 4
#2Zolnerowich N (NIH: National Institutes of Health)
Last. Bo-Ruei Chen (UAB: University of Alabama at Birmingham)
view all 11 authors...
Double-strand break (DSB) repair choice is greatly influenced by the initial processing of DNA ends. 53BP1 limits the formation of recombinogenic single-strand DNA (ssDNA) in BRCA1-deficient cells, leading to defects in homologous recombination (HR). However, the exact mechanisms by which 53BP1 inhibits DSB resection remain unclear. Previous studies have identified two potential pathways: protection against DNA2/EXO1 exonucleases presumably through the Shieldin (SHLD) complex binding to ssDNA, a...
#1Pingping Hou (University of Texas MD Anderson Cancer Center)H-Index: 9
#2Xingdi Ma (University of Texas MD Anderson Cancer Center)H-Index: 3
Last. Xin Zhou (JLU: Jilin University)H-Index: 22
view all 17 authors...
Activating mutations in KRAS (KRAS*) are present in nearly all pancreatic ductal adenocarcinoma (PDAC) cases and critical for tumor maintenance. By using an inducible KRAS* PDAC mouse model, we identified a deubiquitinase USP21-driven resistance mechanism to anti-KRAS* therapy. USP21 promotes KRAS*-independent tumor growth via its regulation of MARK3-induced macropinocytosis, which serves to maintain intracellular amino acid levels for anabolic growth. The USP21-mediated KRAS* bypass, coupled wi...
Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers. Virtually all PDAC harbors an oncogenic mutation in the KRAS gene, making it the prime target for therapy. Most previous attempts to inhibit KRAS directly have been disappointing, but recent success in targeting some KRAS mutants presages a new era in PDAC therapy. Models of PDAC have predicted that identifying KRAS inhibitor resistance mechanisms will be critical. In this issue of Genes & Development, Hou and colleagues (p...
#1Bo Shan (UTSW: University of Texas Southwestern Medical Center)H-Index: 8
#2Mengle Shao (UTSW: University of Texas Southwestern Medical Center)H-Index: 25
Last. Rana K. Gupta (UTSW: University of Texas Southwestern Medical Center)H-Index: 34
view all 6 authors...
The full array of cold-responsive cell types within white adipose tissue that drive thermogenic beige adipocyte biogenesis remains undefined. We demonstrate that acute cold challenge elicits striking transcriptomic changes specifically within DPP4+ PDGFRβ+ adipocyte precursor cells, including a β-adrenergic receptor CREB-mediated induction in the expression of the prothermogenic cytokine, Il33 Doxycycline-inducible deletion of Il33 in PDGFRβ+ cells at the onset of cold exposure attenuates ILC2 a...
#1Hoffman Ra (Duke University)
#2Heather K. MacAlpine (Duke University)H-Index: 8
Last. David M. MacAlpine (Duke University)H-Index: 37
view all 3 authors...
Prior to initiation of DNA replication, the eukaryotic helicase, Mcm2-7, must be activated to unwind DNA at replication start sites in early S phase. To study helicase activation within origin chromatin, we constructed a conditional mutant of the polymerase α subunit Cdc17 (or Pol1) to prevent priming and block replication. Recovery of these cells at permissive conditions resulted in the generation of unreplicated gaps at origins, likely due to helicase activation prior to replication initiation...
The alternative PCNA loader containing CTF18-DCC1-CTF8 facilitates sister chromatid cohesion (SCC) by poorly defined mechanisms. Here we found that in DT40 cells, CTF18 acts complementarily with the Warsaw breakage syndrome DDX11 helicase in mediating SCC and proliferation. We uncover that the lethality and cohesion defects of ctf18 ddx11 mutants are associated with reduced levels of chromatin-bound cohesin and rescued by depletion of WAPL, a cohesin-removal factor. On the contrary, high levels ...
#1Antoine Simoneau (Harvard University)H-Index: 5
#2Rosalinda Xiong (Harvard University)
Last. Lee Zou (Harvard University)H-Index: 53
view all 3 authors...
PARP inhibitor (PARPi) is widely used to treat BRCA1/2-deficient tumors, but why PARPi is more effective than other DNA-damaging drugs is unclear. Here, we show that PARPi generates DNA double-strand breaks (DSBs) predominantly in a trans cell cycle manner. During the first S phase after PARPi exposure, PARPi induces single-stranded DNA (ssDNA) gaps behind DNA replication forks. By trapping PARP on DNA, PARPi prevents the completion of gap repair until the next S phase, leading to collisions of ...
#1Jung Hoon Yoon (UTMB: University of Texas Medical Branch)H-Index: 12
#2Robert E. Johnson (UTMB: University of Texas Medical Branch)H-Index: 29
Last. Satya Prakash (UTMB: University of Texas Medical Branch)H-Index: 110
view all 4 authors...
Chemotherapy with cisplatin becomes limiting due to toxicity and secondary malignancies. In principle, therapeutics could be improved by targeting translesion synthesis (TLS) polymerases (Pols) that promote replication through intrastrand cross-links, the major cisplatin-induced DNA adduct. However, to specifically target malignancies with minimal adverse effects on normal cells, a good understanding of TLS mechanisms in normal versus cancer cells is paramount. We show that in normal cells, TLS ...
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