Plankton populations in Prince William Sound, Alaska, exhibited pronounced seasonal, annual and longer‐period variability in composition and standing stock in response to physically influenced differences in nutrient availability, and possibly currents that modify local biomass by exchanges with water from the bordering Gulf of Alaska. During springs in which early, strong physical stratification developed, intense, short‐lived phytoplankton blooms occurred. These blooms had relatively short residence times in the water column. In contrast, during springs in which slower, weaker stratification developed, phytoplankton blooms were prolonged and took longer to peak. These slower blooms prolonged the period of phytoplankton production, prolonged interaction with the springtime grazing community and led to the incorporation of more organic matter into pelagic food webs. A coupled biological‐physical simulation of plankton production was used to examine the implications of seasonally varying air and mixed‐layer temperatures, surface winds and incident light on the timing, duration, annual production and standing stock of plankton. Our modelling results reproduced the observed characteristics of the springtime production cycle, and the magnitude of zooplankton stocks for the period 1992–97 but not for 1981–91. These results suggest that for most of the 1990s, bottom‐up influences on nutrient supplies controlled levels of primary consumers, whereas for the 11 years before that, other unknown factors dominated this process. We present the results of a comprehensive, multiyear study of relationships between plankton and physical limitations, and a retrospective analysis of earlier conditions to explore the possible causes for these differences.

No abstract

BackgroundCREB3L1 (cAMP-responsive element-binding protein 3-like protein 1), a member of the unfolded protein response, has recently been identified as a metastasis suppressor in both breast and bladder cancer.MethodsQuantitative real time PCR (qPCR) and immunoblotting were used to determine the impact of histone deacetylation and DNA methylation inhibitors on CREB3L1 expression in breast cancer cell lines. Breast cancer cell lines and tumor samples were analyzed similarly, and CREB3L1 gene methylation was determined using sodium bisulfite conversion and DNA sequencing. Immunohistochemistry was used to determine nuclear versus cytoplasmic CREB3L1 protein. Large breast cancer database analyses were carried out to examine relationships between CREB3L1 gene methylation and mRNA expression in addition to CREB3L1 mRNA expression and prognosis.ResultsThis study demonstrates that the low CREB3L1 expression previously seen in highly metastatic breast cancer cell lines is caused in part by epigenetic silencing. Treatment of several highly metastatic breast cancer cell lines that had low CREB3L1 expression with DNA methyltransferase and histone deacetylase inhibitors induced expression of CREB3L1, both mRNA and protein. In human breast tumors, CREB3L1 mRNA expression was upregulated in low and medium-grade tumors, most frequently of the luminal and HER2 amplified subtypes. In contrast, CREB3L1 expression was repressed in high-grade tumors, and its loss was most frequently associated with triple negative breast cancers (TNBCs). Importantly, bioinformatics analyses of tumor databases support these findings, with methylation of the CREB3L1 gene associated with TNBCs, and strongly negatively correlated with CREB3L1 mRNA expression. Decreased CREB3L1 mRNA expression was associated with increased tumor grade and reduced progression-free survival. An immunohistochemistry analysis revealed that low-grade breast tumors frequently had nuclear CREB3L1 protein, in contrast to the high-grade breast tumors in which CREB3L1 was cytoplasmic, suggesting that differential localization may also regulate CREB3L1 effectiveness in metastasis suppression.ConclusionsOur data further strengthens the role for CREB3L1 as a metastasis suppressor in breast cancer and demonstrates that epigenetic silencing is a major regulator of the loss of CREB3L1 expression. We also highlight that CREB3L1 expression is frequently altered in many cancer types suggesting that it could have a broader role in cancer progression and metastasis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13058-016-0672-x) contains supplementary material, which is available to authorized users.

No abstract