Secondary (i.e., heterotrophic or animal) production is a main pathway of energy flow through an ecosystem as it makes energy available to consumers, including humans. Its estimation can play a valuable role in the examination of linkages between ecosystem functions and services. We found that oil and gas platforms off the coast of California have the highest secondary fish production per unit area of seafloor of any marine habitat that has been studied, about an order of magnitude higher than fish communities from other marine ecosystems. Most previous estimates have come from estuarine environments, generally regarded as one of the most productive ecosystems globally. High rates of fish production on these platforms ultimately result from high levels of recruitment and the subsequent growth of primarily rockfish (genus Sebastes) larvae and pelagic juveniles to the substantial amount of complex hardscape habitat created by the platform structure distributed throughout the water column. The platforms have a high ratio of structural surface area to seafloor surface area, resulting in large amounts of habitat for juvenile and adult demersal fishes over a relatively small footprint of seafloor. Understanding the biological implications of these structures will inform policy related to the decommissioning of existing (e.g., oil and gas platforms) and implementation of emerging (e.g., wind, marine hydrokinetic) energy technologies.secondary production | ecosystem-based management | ecosystem services | energy technology | Sebastes

Most human cancers involve either mutational activation of the Ras oncogenic pathway and/or inactivation of the retinoblastoma tumor suppressor (RB) pathway. Paradoxically, tumors that harbor Ras mutations almost invariably retain expression of a wild-type pRB protein. We explain this phenomenon by demonstrating that Ras-induced oncogenic transformation surprisingly depends on functional pRB protein. Cells lacking pRB are less susceptible to the oncogenic actions of H-Ras V12 than wild-type cells and activated Ras has an inhibitory effect on the proliferation of pRB-deficient human tumor cells. In addition, depletion of pRB from Ras-transformed murine cells or human tumor cells that harbor Ras pathway mutations inhibits their proliferation and anchorage-independent growth. In sharp contrast to pRB ؊/؊ 3T3 cells, fibroblasts deficient in other pRB family members (p107 and p130) are more susceptible to Ras-mediated transformation than wild-type 3T3 cells. Moreover, loss of pRB in tumor cells harboring a Ras mutation results in increased expression of p107, and overexpression of p107 but not pRB strongly inhibits proliferation of these tumor cells. Together, these findings suggest that pRB and p107 have distinct roles in Ras-mediated transformation and suggest a novel tumor-suppressive role for p107 in the context of activated Ras.Human tumors arise from an accumulation of genetic changes that result in a disruption of the normal control of several cellular processes, including proliferation, apoptosis, and differentiation. These genetic changes largely include lossof-function mutations in tumor suppressor genes and gain-offunction mutations in proto-oncogenes. The retinoblastoma (Rb) gene was the first tumor suppressor gene to be cloned (22,43) and loss of the Rb gene, originally described as the ratelimiting step in the development of retinoblastomas, has since been found in a variety of other tumor types (28,34,40,74).The retinoblastoma protein (pRB) has been implicated in the regulation of a multitude of cellular processes, such as cell cycle progression and cell death, as well as differentiation (44,68,73). The most clearly established role for pRB may be as a regulator of proliferation (10,16,20,31,36,52,56,71). pRB is thought to control progression through the G 1 phase of the cell cycle by regulating the E2F transcription factor family and the recruitment of chromatin-remodeling complexes to promoter regions (4,6,26,27,65). The ability of pRB to repress E2F-mediated transcription is affected by phosphorylation of pRB by cyclin-dependent kinases, linking pRB to the intricate network that regulates the cell cycle (63). Significantly, alterations in several proteins (loss of the p16 cyclin-dependent kinase inhibitor and amplification of cyclin D or mutation of cdk4) that have been implicated in the regulation of pRB function are also commonly observed in a broad spectrum of tumor types, suggesting that deregulation of the normal pathway in which pRB functions is a common and important event in the development ...

Giant kelp Macrocystis pyrifera is a foundational species that forms a 3-dimensional habitat and supports numerous high-value fisheries species. Constant grazing of kelp holdfasts by overabundant sea urchins causes catastrophic ecological and economic impacts on rocky reefs worldwide. Overgrazing creates urchin barrens that persist for decades in the absence of ecological forcing that would shift the ecosystem back to a kelp-dominated state. Annual surveys of kelp forest and urchin barren sites in the Southern California Bight were performed from 2011 to 2020 to assess changes in kelp forest communities as a result of restoration efforts through sea urchin culling. However, that time period also encompassed a sea urchin mass mortality event. Following drastic reductions of sea urchin densities, rocky reefs returned to a kelp-dominated state within approximately 6 mo and remained stable through the remainder of the study. Benthic cover, fish, and kelp and macroinvertebrate communities inside former urchin barrens became more similar to that of kelp forest reference sites and continued to do so for the next 5 yr. Giant kelp density increased significantly compared to existing kelp forests, while benthic indicators of urchin dominance (i.e. crustose coralline algae and bare rock cover) decreased. Kelp restoration through sea urchin culling essentially mimics sea urchin mass mortality events. If culling can produce similar declines in urchin density, it may be a viable management tool to rapidly restore persistent urchin barrens at moderate spatial scales, while a mass mortality event can drive recovery of kelp forest communities at more extensive spatial scales.

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