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Abstract It has long been observed experimentally that energetic ion-beam irradiation of semiconductor surfaces may lead to spontaneous nanopattern formation. For most ion/target/energy combinations, the patterns appear when the angle of incidence exceeds a critical angle, and the models commonly employed to understand this phenomenon exhibit the same behavioral transition. However, under certain conditions, patterns do not appear for any angle of incidence, suggesting an important mismatch between experiment and theory. Previous work by our group (Swenson and Norris 2018 J. Phys.: Condens. Matter 30 304003) proposed a model incorporating radiation-induced swelling, which is known to occur experimentally, and found that in the analytically-tractable limit of small swelling rates, this effect is stabilizing at all angles of incidence, which may explain the observed suppression of ripples. However, at that time, it was not clear how the proposed model would scale with increased swelling rate. In the present work, we generalize that analysis to the case of arbitrary swelling rates. Using a numerical approach, we find that the stabilization effect persists for arbitrarily large swelling rates, and maintains a stability profile largely similar to that of the small swelling case. Our findings strongly support the inclusion of a swelling mechanism in models of pattern formation under ion beam irradiation, and suggest that the simpler small-swelling limit is an adequate approximation for the full mechanism. They also highlight the need for more—and more detailed—experimental measurements of material stresses during pattern formation. 

Abstract Salinity stress occurs when salt concentration in the environment changes rapidly, for example because of tidal water flow, rainstorms, drought, or evaporation from small bodies of water. However, gradual changes in salt concentration can also cause osmotic stress in aquatic habitats if levels breach thresholds that reduce the fitness of resident organisms. The latter scenario is exemplified by climate change driven salinization of estuaries and by dilution of ocean surface salinity through changes in the water cycle. In this review, we discuss how fish employ the evolutionarily conserved cellular stress response (CSR) to cope with these different forms of salinity stress. Macromolecular damage is identified as the cause of impaired physiological performance during salinity stress and serves as the signal for inducing a CSR. Basic aspects of the CSR have been observed in fish exposed to salinity stress, including repair and protection of cellular macromolecules, reallocation of energy, cell cycle arrest, and in severe cases, programmed cell death. Osmosensing and signal transduction events that regulate these aspects of the CSR provide a link between environmental salinity and adaptive physiological change required for survival. The CSR has evolved to broaden the range of salinities tolerated by certain euryhaline fish species, but is constrained in stenohaline species that are sensitive to changes in environmental salinity. Knowledge of how the CSR diverges between euryhaline and stenohaline fish enables understanding of physiological mechanisms that underlie salt tolerance and facilitates predictions as to the relative vulnerabilities of different fish species to a rapidly changing hydrosphere. 

Abstract Inducible prey defences occur when organisms undergo plastic changes in phenotype to reduce predation risk. When predation pressure varies persistently over space or time, such as when predator and prey co‐occur over only part of their biogeographic ranges, prey populations can become locally adapted in their inducible defences. In California estuaries, native Olympia oyster (Ostrea lurida) populations have evolved disparate phenotypic responses to an invasive predator, the Atlantic oyster drill (Urosalpinx cinerea). In this study, oysters from an estuary with drills, and oysters from an estuary without drills, were reared for two generations in a laboratory common garden, and subsequently exposed to cues from Atlantic drills. Comparative proteomics was then used to investigate molecular mechanisms underlying conserved and divergent aspects of their inducible defences. Both populations developed smaller, thicker, and harder shells after drill exposure, and these changes in shell phenotype were associated with upregulation of calcium transport proteins that could influence biomineralization. Inducible defences evolve in part because defended phenotypes incur fitness costs when predation risk is low. Immune proteins were downregulated by both oyster populations after exposure to drills, implying a trade‐off between biomineralization and immune function. Following drill exposure, oysters from the population that co‐occurs with drills grew smaller shells than oysters inhabiting the estuary not yet invaded by the predator. Variation in the response to drills between populations was associated with isoform‐specific protein expression. This trend suggests that a stronger inducible defence response evolved in oysters that co‐occur with drills through modification of an existing mechanism.