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Abstract

Acquisition of the classically conditioned eyeblink response is generally regarded as one of the most basic forms of associative learning. A great deal is known about how the brain encodes this simple form of learning, so that performance of this task may be an indirect indicator of brain functioning. Individual differences in response acquisition have been revealed, but largely ignored, in the research literature. We tested the temporal stability and familial origins of these individual differences using a classic twin study design. Results reveal substantial individual differences in acquisition of the conditioned eyeblink response. These differences are stable across brief retest, and differences in response acquisition exhibit familial aggregation, apparently due, in part, to genetic resemblance.

Saccharomyces cerevisiae Sin3p facilitates DNA double-strand break repair

“…These results provide further evidence that Sin3p facilitates NHEJ but not HR. These conclusions are thus consistent with sin3⌬ mutants being hypersensitive to phleomycin, which induces DSBs throughout the cell cycle, but not to high levels of HU, which produces DSBs mainly in S phase, where they are thought to be repaired mainly by HR (43).…”

“…Phleomycin causes DNA DSBs (41), whereas HU leads to depletion of the deoxyribonucleotide pool that in turn slows down S-phase progression and activates the DNA replication checkpoint (42). Furthermore, high levels of HU (e.g., 200 mM) cause the formation of S phase-specific DNA DSBs (43). In addition, we treated cells with UV light, which causes cyclobutane pyrimidine dimers and 6-4 photoproducts that are repaired primarily by nucleotide excision repair (44).…”

RecA-dependent mutants in Escherichia coli reveal strategies to avoid chromosomal fragmentation

“…The idea of this screen has been adopted from the work of Holm and colleagues (37)(38)(39), who successfully used a similar screen to look for synthetic lethals in the yeast Saccharomyces cerevisiae. We worked in the DH5␣ strain of E. coli, because it forms compact and almost colorless colonies on MacConkey plates.…”

DNA replication meets genetic exchange: Chromosomal damage and its repair by homologous recombination

“…Mec1 is a key DNA damage checkpoint protein in S. cerevisiae; mec1-srf mutants depend on RAD52 and accumulate singlestrand interruptions in the newly synthesized DNA, apparently because of their inability to lift the inhibition of ribonucleotide reductase (82). When budding yeast cells are treated with hydroxyurea to inhibit ribonucleotide reductase, they also accumulate single-strand interruptions in DNA and also become dependent on RAD52 (82).…”

“…When budding yeast cells are treated with hydroxyurea to inhibit ribonucleotide reductase, they also accumulate single-strand interruptions in DNA and also become dependent on RAD52 (82). DNA of rad52 mutants, treated with hydroxyurea, is fragmented, suggesting conversion of singlestrand breaks into double-strand breaks (82).…”