Publications by authors named "Peter M Garber"
Article Synopsis
- Double-stranded DNA breaks (DSBs) are serious DNA damage events that can result in chromosome loss and mutations, triggering a complex repair response.
- Proteins are recruited to the DSB site to initiate repair through either non-homologous end-joining (NHEJ) or homologous recombination (HR), with checkpoint activation mediated by specific kinases.
- Recent yeast studies reveal that the protein localization to DSBs follows a specific sequence, starting with Tel1 and NHEJ proteins for initial signaling, transitioning to Mec1 and HR proteins, influenced by the cell cycle stage.
The MAD2-dependent spindle checkpoint blocks anaphase until all chromosomes have achieved successful bipolar attachment to the mitotic spindle. The DNA damage and DNA replication checkpoints block anaphase in response to DNA lesions that may include single-stranded DNA and stalled replication forks. Many of the same conditions that activate the DNA damage and DNA replication checkpoints also activated the spindle checkpoint.
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