scholarly journals The genetics and the molecular functions of the PREP1 homeodomain transcription factor

2018 ◽  
Vol 62 (11-12) ◽  
pp. 819-825 ◽  
Author(s):  
Divya Purushothaman ◽  
Francesco Blasi
Keyword(s):  
Dna Damage ◽  
Transcription Factor ◽  
Dna Replication ◽  
Tumor Suppressor ◽  
Embryonic Development ◽  
Cellular Function ◽  
Mutant Mice ◽  
Homeodomain Transcription Factor ◽  
Molecular Functions

Prep1 (pKnox1) is a homeodomain transcription factor of the TALE superclass whose members can act as co-factors of Hox. Prep1 is essential for embryogenesis, but in the adult it also acts as a tumor suppressor. We describe and analyze here the available mutant mice, their phenotypes and a few discordant cases. Moreover we specify the basic rules underlying the binding of Prep1 and its TALE partners to DNA, and their plasticity during embryonic development. We finally review recent data on Prep1 which indicate a very basic cellular function at the level of DNA replication and DNA damage.

scholarly journals Homeodomain transcription factor and tumor suppressor Prep1 is required to maintain genomic stability

2011 ◽  
Vol 108 (29) ◽  
pp. E314-E322 ◽  
Author(s):  
G. Iotti ◽  
E. Longobardi ◽  
S. Masella ◽  
L. Dardaei ◽  
F. De Santis ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Tumor Suppressor ◽  
Genomic Stability ◽  
Homeodomain Transcription Factor

scholarly journals Mouse Zygotes Respond to Severe Sperm DNA Damage by Delaying Paternal DNA Replication and Embryonic Development

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e56385 ◽  
Author(s):  
Joanna E. Gawecka ◽  
Joel Marh ◽  
Michael Ortega ◽  
Yasuhiro Yamauchi ◽  
Monika A. Ward ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Replication ◽  
Embryonic Development ◽  
Sperm Dna Damage ◽  
Sperm Dna ◽  
Mouse Zygotes

scholarly journals A homeodomain transcription factor regulates the DNA replication checkpoint in yeast

Cell Cycle ◽  
2011 ◽  
Vol 10 (4) ◽  
pp. 664-670 ◽  
Author(s):  
Frances S. Purtill ◽  
Simon K. Whitehall ◽  
Emma S. Williams ◽  
Christopher J. McInerny ◽  
Andrew D. Sharrocks ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Dna Replication ◽  
Replication Checkpoint ◽  
Homeodomain Transcription Factor ◽  
Dna Replication Checkpoint

scholarly journals DNA damage tolerance pathway involving DNA polymerase ι and the tumor suppressor p53 regulates DNA replication fork progression

2016 ◽  
Vol 113 (30) ◽  
pp. E4311-E4319 ◽  
Author(s):  
Stephanie Hampp ◽  
Tina Kiessling ◽  
Kerstin Buechle ◽  
Sabrina F. Mansilla ◽  
Jürgen Thomale ◽  
...  
Keyword(s):  
Dna Damage ◽  
Dna Replication ◽  
Tumor Suppressor ◽  
Damage Tolerance ◽  
Replication Stress ◽  
Nuclear Antigen ◽  
Replication Forks ◽  
Tumor Suppressor P53 ◽  
Dna Damage Tolerance ◽  
Direct Role

DNA damage tolerance facilitates the progression of replication forks that have encountered obstacles on the template strands. It involves either translesion DNA synthesis initiated by proliferating cell nuclear antigen monoubiquitination or less well-characterized fork reversal and template switch mechanisms. Herein, we characterize a novel tolerance pathway requiring the tumor suppressor p53, the translesion polymerase ι (POLι), the ubiquitin ligase Rad5-related helicase-like transcription factor (HLTF), and the SWI/SNF catalytic subunit (SNF2) translocase zinc finger ran-binding domain containing 3 (ZRANB3). This novel p53 activity is lost in the exonuclease-deficient but transcriptionally active p53(H115N) mutant. Wild-type p53, but not p53(H115N), associates with POLι in vivo. Strikingly, the concerted action of p53 and POLι decelerates nascent DNA elongation and promotes HLTF/ZRANB3-dependent recombination during unperturbed DNA replication. Particularly after cross-linker–induced replication stress, p53 and POLι also act together to promote meiotic recombination enzyme 11 (MRE11)-dependent accumulation of (phospho-)replication protein A (RPA)-coated ssDNA. These results implicate a direct role of p53 in the processing of replication forks encountering obstacles on the template strand. Our findings define an unprecedented function of p53 and POLι in the DNA damage response to endogenous or exogenous replication stress.

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