Bloom syndrome, characterized by a predisposition to cancer, is caused by mutation of the RecQ DNA helicase gene BLM. The precise function of BLM remains unclear. Previous research suggested that Drosophila BLM functions in the repair of DNA double-strand breaks. Most double-strand breaks in flies are repaired by homologous recombination through the synthesis-dependent strand-annealing pathway. Here, we demonstrate that Drosophila BLM mutants are severely impaired in their ability to carry out repair DNA synthesis during synthesis-dependent strand annealing. Consequently, repair in the mutants is completed by error-prone pathways that create large deletions. These results suggest a model in which BLM maintains genomic stability by promoting efficient repair DNA synthesis and thereby pre

/pdf/drosophila-blm-in-double-strand-break-repair-by-synthesis-4z6bn7ecm9.pdf

Drosophila BLM in Double-Strand Break Repair by Synthesis-

Homologous recombination is a DNA repair mechanism that uses the genetic information of a homologous DNA sequence as template for repair of a DNA break. The genetic consequences of recombination depend on the choice of the molecule used as template. While sister-chromatid recombination (SCR), which uses as template for repair the identical and intact sister chromatid, preserves genome integrity, allelic and ectopic recombination can compromise it. SCR is, thus, the most secure mechanism of recombinational repair. This, together with the fact that most DNA breaks may appear spontaneously during replication, makes SCR the major recombination event occurring in mitotic cells from yeast to mammals. Given its physiological relevance, we review here the current knowledge about the mechanism(s) of SCR as well as the genetic and molecular factors controlling it, and how this knowledge open new perspectives to our understanding of genome dynamics.

Sister chromatid recombination

Homologous recombination (HR) is one of the key mechanisms responsible for the repair of DNA double-strand breaks (DSBs), including those that occur during DNA replication. Recent studies in yeast and mammals have uncovered that the SMC complexes cohesins and Smc5-Smc6 are recruited to induced DSBs, and play a role in the maintenance of genome stability by favouring SCR as the main recombinational DSB repair mechanism. These new results raise intriguing questions such as whether SMC proteins might play a functional role at collapsed replication forks, which may represent the main source of spontaneous recombinogenic damage. A deeper knowledge of the role of SMC proteins in DSB repair should contribute to a better understanding of chromosome dynamics and stability.

http://digital.csic.es/bitstream/10261/4097/3/SMC_2007.pdf

SMC proteins, new players in the maintenance of genomic stability

Topics in Current Genetics publishes review articles of wide interest in volumes that centre around a specific topic in genetics, genomics as well as cell, molecular and developmental biology. Particular emphasis is placed on the comparison of several model organisms. Volume editors are invited by the series editors for special topics, but further suggestions for volume topics are highly welcomed.  Each volume is edited by one or several acknowledged leaders in the field, who ensure the highest standard of content and presentation. All contributions are peer-reviewed.  All volumes of Topics in Current Genetics are published as eBooks as well as in print. The eBook format gives the volumes an increased global readership and enhanced visibility.

Topics in current genetics

Sister chromatids are preferred substrates for the recombinational repair of DNA lesions. Sister chromatid recombination (SCR) results in the exchange of genetic information between newly replicated chromatids and ensures that DNA lesions are either tolerated or repaired. Faulty recombinational repair has been correlated to several genetic diseases, including Bloom's syndrome, inheritable breast cancer (BRCA1 and BRCA2), and Fanconi's Anemia. One approach to understand SCR mechanisms is to clarify the SCR phenotypes in mutants defective in well-conserve d radiation repair (RAD) genes. These RAD genes include those that participate directly in the recombinational repair of DSBs, known as the RAD51 subgroup, and those that participate in the processing of the DNA break, known as the RAD50 subgroup. A systematic analysis of SCR recombination phenotypes in rad mutants revealed multiple pathways for spontaneous and DNA damage-associated SCR in yeast. Studies focused on vertebrate RAD51 genes have suggested similar pathways. In this review, we shall discuss methods for detecting SCR, recombination mechanisms that generate SCR, mammalian and yeast genes that participate in SCR, and genetic diseases characterized by SCR phenotypes.

Genetic Control of Sister Chromatid Recombination: The Role of Radiation Repair (RAD) Genes

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Genetic Control of Sister Chromatid Recombination: The Role of Radiation Repair (RAD) Genes