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The RAD51 gene of Saccharomyces cerevisiae is required both for recombination and for the repair of DNA damage caused by X rays. Here we report the sequence and transcriptional regulation of this gene. The RAD51 protein shares significant homology (-50%) over a 70-amino-acid stretch with the RAD57 protein (J. A. Kans and R. K. Mortimer, Gene 105:139-140, 1991), the product of another yeast recombinational repair gene, and also moderate (-27%), but potentially significant, homology with the bacterial RecA protein. The homologies cover a region that encodes a putative nucleotide binding site of the RAD51 protein. Sequences upstream of the coding region for RAD51 protein share homology with the damage response sequence element of RAD54, an upstream activating sequence required for damage regulation of the RADS4 transcript, and also contain two sites for restriction enzyme MluI; the presence of MluI restriction sites has been associated with cell cycle regulation. A 1.6-kb transcript corresponding to RAD51 was observed, and levels of this transcript increased rapidly after exposure to relatively low doses of X rays. Additionally, RAD51 transcript levels were found to vary throughout the cell cycle, peaking in late GI to early S. The observed cell cycle regulation is consistent with that of a group of genes involved primarily in DNA synthesis and replication which are thought to be coordinately cell cycle regulated. Cells arrested in early G1 were still capable of increasing levels of RAD51 transcript after irradiation, indicating that increased RAD)5 transcript levels after X-ray exposure are not solely due to an X-ray-induced cessation of the cell cycle at a period when the level of RADS expression is normally high.Organisms are able to sense and respond to DNA damage caused by a variety of environmental agents; mutations which block these abilities can lead to a loss of growth capacity and eventually to cell death. In the yeast Saccharomyces cerevisiae, genetic analyses of mutations conferring an increase in sensitivity to irradiation have defined three epistasis groups, the RAD3, RAD6, and RAD52 groups, which are thought to reflect three repair pathways (18; for reviews, see references 15, 16, and 20). The RAD3 group, which is characterized by mutations that confer a high degree of sensitivity to UV radiation, are known to act in excision repair of damaged DNA. The RAD6 group is required for resistance to both UV and X rays; a subset of these genes is believed to act in a pathway of postreplication repair. The RAD52 group, made up of the genes RAD50 to RADS7, is required for resistance to X-ray radiation.Three genes in the RADSO-to-RAD57 group, RADS1, RAD52, and RAD54, form a subset displaying a number of similar phenotypes which indicate roles in general recombination and in DNA repair that involves recombinational activity (16). Mutations in any one of these three loci confer the most extreme sensitivity to X rays of any of the yeast rad mutations but only slight sensitivity to UV (16,18,19). Damage arising fro...

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ABSTRACT. Recently, an approach for global sustainability, the planetary-boundary approach (PBA), has been proposed, which combines the concept of tipping points with global-scale sustainability indicators. The PBA could represent a significant step forward in monitoring and managing known and suspected global sustainability criteria. However, as the authors of the PBA describe, the approach faces numerous and fundamental challenges that must be addressed, including successful identification of key global sustainability metrics and their tipping points, as well as the coordination of systemic individual and institutional actions that are required to address the sustainability challenges highlighted. We apply a previously published framework for systematic and strategic development toward a robust basic definition of sustainability, i.e., the framework for strategic sustainable development (FSSD), to improve and inform the PBA. The FSSD includes basic principles for sustainability, and logical guidelines for how to approach their fulfillment. It is aimed at preventing unsustainable behavior at both the micro, e.g., individual firm, and macro, i.e., global, levels, even when specific global sustainability symptoms and metrics are not yet well understood or even known. Whereas the PBA seeks to estimate how far the biosphere can be driven away from a "normal" or "natural" state before tipping points are reached, because of ongoing violations of basic sustainability principles, the FSSD allows for individual planners to move systematically toward sustainability before all impacts from not doing so, or their respective tipping points, are known. Critical weaknesses in the PBA can, thus, be overcome by a combined approach, significantly increasing both the applicability and efficacy of the PBA, as well as informing strategies developed in line with the FSSD, e.g., by providing a "global warning system" to help prioritize strategic actions highlighted by the FSSD. Thus, although ongoing monitoring of known and suspected global sustainability metrics and their possible tipping points is a critical part of the evolving sustainability landscape, effective and timely utilization of planetary-boundary information on multiple scales requires coupling to a strategic approach that makes the underlying sustainability principles explicit and includes strategic guidelines to approach them. Outside of such a rigorous and systems-based context, the PBA, even given its global scale, risks leading individual organizations or planners to (i) focus on "shares" of, e.g., pollution within the PBs and negotiations to get as high proportion of such as possible, and/or (ii) awaiting data on PBs when such do not yet exist before they act, and/or (iii) find it difficult to manage uncertainties of the data once such have arrived. If global sustainability problems are to be solved, it is important that each actor recognizes the benefits, not the least self-benefits, of designing and executing strategies toward a principled and scientifically rob...

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The RAD51 gene of Saccharomyces cerevisiae is required both for recombination and for the repair of DNA damage caused by X rays. Here we report the sequence and transcriptional regulation of this gene. The RAD51 protein shares significant homology (approximately 50%) over a 70-amino-acid with the RAD57 protein (J.A. Kans and R.K. Mortimer, Gene 105:139-140, 1991), the product of another yeast recombinational repair gene, and also moderate (approximately 27%), but potentially significant, homology with the bacterial RecA protein. The homologies cover a region that encodes a putative nucleotide binding site of the RAD51 protein. Sequences upstream of the coding region for RAD51 protein share homology with the damage response sequence element of RAD54, an upstream activating sequence required for damage regulation of the RAD54 transcript, and also contain two sites for restriction enzyme MluI; the presence of MluI restriction sites has been associated with cell cycle regulation. A 1.6-kb transcript corresponding to RAD51 was observed, and levels of this transcript increased rapidly after exposure to relatively low doses of X-rays. Additionally, RAD51 transcript levels were found to that of a group of genes involved primarily in DNA synthesis and replication which are thought to be coordinately cell cycle regulated. Cells arrested in early G1 were still capable of increasing levels of RAD51 transcript after irradiation, indicating that increased RAD51 transcript levels after X-ray exposure are not solely due to an X-ray-induced cessation of the cell cycle at a period when the level of RAD51 expression is normally high.