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Extra resources for Cell Cycle Control: Mechanisms and Protocols (Methods in Molecular Biology)
In yeast, several signaling pathways, including the PKA and TOR pathways, are proposed to mediate nutrient control of the cell cycle, and the unifying characteristic of these pathways is that they control ribosome biogenesis, such that translational activity serves as a cellular indicator of nutritional status. Another mechanism by which cells may coordinate cell size with cell cycle progression is via monitoring of cell geometry. The fission yeast S. pombe is shaped like a cylinder and grows lengthwise prior to division.
Activated Cds1/Chk2 then stabilizes the stalled replisome by phosphorylation of several subunits, notably the MCM helicase [59, 60]. In budding yeast, the Rad53 kinase serves the function of Cds1/Chk2. Like Cds1/Chk2, Rad53 has an N-terminal FHA domain followed by a kinase domain. However, Rad53 has an additional C-terminal FHA domain not seen in Cds1 that is important in its activation by DNA damage . 4 S–M Dependency Upon stabilization, the replisome may stay in position until the blockade is removed or dNTPs restored.
Further, another kinase known as Dun1 is activated in budding Cell Cycle Checkpoints 33 yeast , which controls transcriptional responses to DNA damage including activation of ribonucleotide reductase, the enzyme required for dNTP synthesis. In higher organisms, the transcription factor p53 is a critical component of DNA damage checkpoints , particularly in G1 phase. p53 is regulated by a plethora of posttranslational modifications, including N-terminal phosphorylation on serine-15, which is catalyzed by ATR and its cousins ATM (Ataxia Telangiectasia Mutated) and DNA-PKcs (DNA-dependent protein kinase, catalytic subunit).