Double-strand break repair by interchromosomal recombination: suppression of chromosomal translocations

Article Abstract:

To find out directly whether recombinational repair of double-strand breaks (DSBs) can take place between heterologous chromosomes and can lead to chromosomal rearrangements in mammalian cells, an ES cell system was used to analyze recombination between repeats on heterologous chromosomes. Recombination is induced at least 1000-fold after introduction of a DSB in one repeat. Almost all recombinants repaired the DSB by gene conversion in which a small amount of sequence information was moved from the unbroken chromosome to the broken one. Remaining recombinants transferred a larger amount of information, but no chromosomal aberrations were seen. Cells from mammals can search throughout the genome for sequences suitable for repair of a DSB. Crossover events would have led to translocations, but they were not seen. It seems a model with recombination coupled to replication is valid.

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Crystal structure of a GCN5-related N-acetyltransferase: Serratia marcescens aminoglycoside 3-N-acetyltransferase

Article Abstract:

The 2.3 A resolution of the x-ray structure of the Serratia marcescens aminoglycoside 3-N-acetyltransferase was determined in an experiment. Results showed that the single domain alpha/beta protein was similar to a cupped right hand wrapped around a cylinder. This protein was found to be composed of six-stranded beta sheet sandwiched between four alpha helices. The structure represents the catalytic core of the enzyme superfamily and includes all four conserved GNAT motifs.

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DNA damage activates p53 through a phosphorylation-acetylation cascade

Article Abstract:

DNA damage appears to enhance p53 activity as a transcription factor partly through carboxy-terminal acetylation that is itself directed by amino-terminal phosphorylation. The activation involves a phosphorylation-acetylation cascade. In vitro p53 is acetylated at different sites by two histone acetyltransferases (HATs), p300 and PCAF, coactivators. At both sites the acetylations enhance sequence-specific DNA binding.

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