Legacy of past exposure to hypoxia and warming regulates an ecosystem service provided by oysters

Climate change is having substantial impacts on organism fitness and ability to deliver critical ecosystem services, but these effects are often examined only in response to current environments. Past exposure to stress can also affect individuals via carryover effects, and whether these effects scale from individuals to influence ecosystem function and services is unknown. We explored within-generation carryover effects of two coastal climate change stressors—hypoxia and warming—on oyster (Crassostrea virginica) growth and nitrogen bioassimilation, an important ecosystem service. Oysters were exposed to a factorial combination of two temperature and two diel-cycling dissolved oxygen treatments at 3-months-old and again 1 year later. Carryover effects of hypoxia and warming influenced oyster growth and nitrogen storage in complex and context-dependent ways. When operating, carryover effects of single stressors generally reduced oyster nitrogen bioassimilation and relative investment in tissue versus shell growth, particularly in warm environments, while early life exposure to multiple stressors generally allowed oysters to perform as well as control oysters. When extrapolated to the reef scale, carryover effects decreased nitrogen stored by modeled oyster reefs in most conditions, with reductions as large as 41%, a substantial decline in a critical ecosystem service. In some scenarios, however, carryover effects increased nitrogen storage by modeled oyster reefs, again highlighting the complexity of these effects. Hence, even brief exposure to climate change stressors early in life may have persistent effects on an ecosystem service 1 year later. Our results show for the first time that within-generation carryover effects on individual phenotypes can impact processes at the ecosystem scale and may therefore be an overlooked factor determining ecosystem service delivery in response to anthropogenic change.     

Accelerated loss of telomeric repeats may not explain accelerated replicative decline of Werner syndrome cells

The Werner syndrome (WS) is characterized by the premature onset and accelerated rate of development of major geriatric disorders, including atherosclerosis, diabetes mellitus, osteoporosis, ocular cataracts, and various neoplasms. Cultures of WS skin-fibroblastlike cells have been previously shown to undergo accelerated rates of decline of their replicative potentials and to exhibit variegated chromosomal translocations and deletions. Since the replicative decline of normal somatic cells is associated with a loss of telomeric repeats, we investigated the kinetics of telomeric repeat loss in WS cells. The mean length of telomere restriction fragments (TRF) from the earliest passages of WS cells studied was not shorter than those of controls, possibly reflecting selective pressure for subsets of cells with relatively high residual replicative capacity. Statistical evidence indicated an accelerated shortening of TRF length in serially passaged WS cultures, but the mean TRF lengths of WS cultures that had ceased replicating were significantly longer than those of senescent controls. Thus, while accelerated loss of telomeric repeats could potentially explain the rapid decline in proliferation of WS cells, it is possible that WS cells exit the cell cycle via mechanisms that differ from those of replicatively senescent cells from control subjects.     

A cloning assay for 6-thioguanine resistance provides evidence against certain somatic mutational theories of aging

The frequencies of 6-thioguanine-resistant primary clones from the kidneys and skeletal muscles of aging male cohorts of two F1 hybrid strains of Mus musculus varied from 0.59 to 10.96 X 10(-5) and did not increase as a function of donor age (up to 40 months). Resistant clones were shown to be severely deficient in the activity of hypoxanthine-guanine phosphoribosyltransferase (EC 2.4.2.8). These deficiencies presumably resulted from molecular alterations at this X-linked locus, including point mutations. No alterations of the X-chromosome were observed at the level of the light microscope. These results are inconsistent with predictions of the intrinsic mutagenesis and protein synthesis error catastrophe theories of aging. They do not rule out, however, somatic mutational theories that invoke comparatively large-scale chromosomal lesions, many of which would be likely to be lethal at the cellular level.