Seasonal oscillations in water exchange between aquifers and the coastal ocean

Ground water of both terrestrial and marine origin flows into coastal surface waters as submarine groundwater discharge, and constitutes an important source of nutrients, contaminants and trace elements to the coastal ocean. Large saline discharges have been observed by direct measurements and inferred from geochemical tracers, but sufficient seawater inflow has not been observed to balance this outflow. Geochemical tracers also suggest a time lag between changes in submarine groundwater discharge rates and the seasonal oscillations of inland recharge that drive groundwater flow towards the coast. Here we use measurements of hydraulic gradients and offshore fluxes taken at Waquoit Bay, Massachusetts, together with a modelling study of a generalized coastal groundwater system to show that a shift in the freshwater-saltwater interface-controlled by seasonal changes in water table elevation-can explain large saline discharges that lag inland recharge cycles. We find that sea water is drawn into aquifers as the freshwater-saltwater interface moves landward during winter, and discharges back into coastal waters as the interface moves seaward in summer. Our results demonstrate the connection between the seasonal hydrologic cycle inland and the saline groundwater system in coastal aquifers, and suggest a potentially important seasonality in the chemical loading of coastal waters.     

A DNA damage checkpoint response in telomere-initiated senescence

Most human somatic cells can undergo only a limited number of population doublings in vitro. This exhaustion of proliferative potential, called senescence, can be triggered when telomeres--the ends of linear chromosomes-cannot fulfil their normal protective functions. Here we show that senescent human fibroblasts display molecular markers characteristic of cells bearing DNA double-strand breaks. These markers include nuclear foci of phosphorylated histone H2AX and their co-localization with DNA repair and DNA damage checkpoint factors such as 53BP1, MDC1 and NBS1. We also show that senescent cells contain activated forms of the DNA damage checkpoint kinases CHK1 and CHK2. Furthermore, by chromatin immunoprecipitation and whole-genome scanning approaches, we show that the chromosome ends of senescent cells directly contribute to the DNA damage response, and that uncapped telomeres directly associate with many, but not all, DNA damage response proteins. Finally, we show that inactivation of DNA damage checkpoint kinases in senescent cells can restore cell-cycle progression into S phase. Thus, we propose that telomere-initiated senescence reflects a DNA damage checkpoint response that is activated with a direct contribution from dysfunctional telomeres.