DNA repair mechanisms are essential for the maintenance of genomic integrity. Disruption of gene products responsible for DNA repair can result in chromosomal damage. Improperly repaired chromosomal damage can result in the loss of chromosomes or the generation of chromosomal deletions or translocations, which can lead to tumorigenesis. The MYC protooncogene is a transcription factor whose overexpression is frequently associated with human neoplasia. MYC has not been previously implicated in a role in DNA repair. Here we report that the overexpression of MYC disrupts the repair of double-strand DNA breaks, resulting in a several-magnitude increase in chromosomal breaks and translocations. We found that MYC inhibited the repair of ␥ irradiation DNA breaks in normal human cells and blocked the repair of a single double-strand break engineered to occur in an immortal cell line. By spectral karyotypic analysis, we found that MYC even within one cell division cycle resulted in a several-magnitude increase in the frequency of chromosomal breaks and translocations in normal human cells. Hence, MYC overexpression may be a previously undescribed example of a dominant mutator that may fuel tumorigenesis by inducing chromosomal damage.M any genes have been identified that are responsible for repairing DNA breaks and preserving chromosomal integrity (1-3). The loss of function of some of these genes can result in widespread chromosomal damage and contribute to tumorigenesis (4-6). In mammalian cells, double-strand DNA breaks (DSBs) are repaired by homology-directed recombination (HDR), nonhomologous end joining (NHEJ), and singlestrand annealing (SSA) (7). Defects in any of these repair mechanisms can result in chromosomal breaks, fusions, and translocations (8). Many human cancers exhibit characteristic chromosomal translocations thought to be responsible for tumorigenesis (9). The mechanisms by which these chromosomal translocations occur are not clear.MYC is a protooncogene that normally regulates cellular growth and proliferation and in some contexts induces apoptosis (10-12). MYC overexpression is thought to cause tumorigenesis by promoting unrestrained cellular proliferation and blocking differentiation. MYC overexpression may also contribute to tumorigenesis by inducing genomic destabilization (13-15). The genomic damage induced by MYC can be broadly grouped into two classes of abnormalities. First, overexpression of MYC induces loss of chromosomal integrity associated with chromosomal aberrations such as gene amplifications, double minutes, and fusions. Second, MYC overexpression can cause inappropriate DNA replication, resulting in endoreduplication.We speculated that the former type of genomic abnormalities might be caused by defects in the repair of DSBs. Here we demonstrate that MYC overexpression disrupts the repair of DSBs. Moreover, we show that MYC overexpression in normal human cells results in a several-magnitude increase in chromosomal breaks and translocations. Hence, MYC may be a previously undescribed ...

The wider effects of fishing on marine ecosystems have become the focus of growing concern among scientists, fisheries managers and the fishing industry. The present review examines the role of habitat structure and habitat heterogeneity in marine ecosystems, and the effects of fishing (i.e. trawling and dredging) on these two components of habitat complexity. Three examples from New Zealand and Australia are considered, where available evidence suggests that fishing has been associated with the degradation or loss of habitat structure through the removal of large epibenthic organisms, with concomitant effects on fish species which occupy these habitats. With ever‐increasing demands on fish‐stocks and the need for sustainable use of fisheries resources, new approaches to fisheries management are needed. Fisheries management needs to address the sustainability of fish‐stocks while minimizing the direct and indirect impacts of fishing on other components of the ecosystem. Two long‐term management tools for mitigating degradation or loss of habitat structure while maintaining healthy sustainable fisheries which are increasingly considered by fisheries scientists and managers are: (1) protective habitat management, which involves the designation of protected marine and coastal areas which are afforded some level of protection from fishing; and (2) habitat restoration, whereby important habitat and ecological functions are restored following the loss of habitat and/or resources. Nevertheless, the protection of marine and coastal areas, and habitat restoration should not be seen as solutions replacing conventional management approaches, but need to be components of an integrated programme of coastal zone and fisheries management. A number of recent international fisheries agreements have specifically identified the need to provide for habitat protection and restoration to ensure long‐term sustainability of fisheries. The protection and restoration of habitat are also common components of fisheries management programs under national fisheries law and policy.

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Commercial fishing is one of the most important human impacts on the marine benthic environment. One such impact is through disturbance to benthic habitats as fishing gear (trawls and dredges) are dragged across the seafloor. While the direct effects of such an impact on benthic communities appear obvious, the magnitude of the effects has been very difficult to evaluate. Experimental fishing‐disturbance studies have demonstrated changes in small areas; however, the broader scale implications attributing these changes to fishing impacts are based on long‐term data and have been considered equivocal. By testing a series of a priori predictions derived from the literature (mainly results of small‐scale experiments), we attempted to identify changes in benthic communities at the regional scale that could be attributed to commercial fishing. Samples along a putative gradient of fishing pressure were collected from 18 sites in the Hauraki Gulf, New Zealand. These sites varied in water depth from ∼17 to 35 m and in sediment characteristics from ∼1 to 48% mud and from 3 to 8.5 μg chlorophyll a/cm3. Video transects were used for counting large epifauna and grab/suction dredge and core sampling were used for collecting macrofauna. After accounting for the effects of location and sediment characteristics, 15–20% of the variability in the macrofauna community composition sampled in the cores and grab/suction dredge samples was attributed to fishing. With decreasing fishing pressure we observed increases in the density of echinoderms, long‐lived surface dwellers, total number of species and individuals, and the Shannon‐Weiner diversity index. In addition, there were decreases in the density of deposit feeders, small opportunists, and the ratio of small to large individuals of the infaunal heart urchin, Echinocardium australe. The effects of fishing on the larger macrofauna collected from the grab/suction dredge samples were not as clear. However, changes in the predicted direction in epifaunal density and the total number of individuals were demonstrated. As predicted, decreased fishing pressure significantly increased the density of large epifauna observed in video transects. Our data provide evidence of broad‐scale changes in benthic communities that can be directly related to fishing. As these changes were identifiable over broad spatial scales they are likely to have important ramifications for ecosystem management and the development of sustainable fisheries.