Parent-off spring associations in wintering brent geese: parental investment or mutual assistance?

The continued parent-offspring associations in the Eastern Canadian High Arctic light-bellied brent goose Branta bernicla hrota was examined to determine whether this is an example of continued parental investment or mutual assistance. Adults with juveniles spend more than twice as much time being vigilant and aggressive than do those without offspring. The loss of a partner, however, does not result in the remaining parent increasing parental care but does result in increased 'self-care' by the juveniles. Neither parents nor single-parent juveniles appear to pay an energetic cost relative to non-parental adults and two-parent juveniles, respectively. Differences in the feeding distribution of parents and non-parents and equivalent or better physical condition suggests that families are able to maintain access to a superior food supply over the winter. Passive 'assistance' by juveniles may assist in maintaining this position in favoured areas, and this is achieved with little overt aggression. The present study thus provides no data that show a net cost to parents by remaining with their juveniles over the winter period. Thus, mutual assistance might be a better explanation of the prolonged association rather than a period of parental investment with an overall cost.

JMJD6 is a driver of cellular proliferation and motility and a marker of poor prognosis in breast cancer

We developed an analytic strategy that correlates gene expression and clinical outcomes as a means to identify novel candidate oncogenes operative in breast cancer. This analysis, followed by functional characterization, resulted in the identification of Jumonji Domain Containing 6 (JMJD6) protein as a novel driver of oncogenic properties in breast cancer.

Impact of oncogenic driver mutations on feedback between the PI3K and MEK pathways in cancer cells

Inhibition of the PI3K (phosphoinositide 3-kinase)/Akt/mTORC1 (mammalian target of rapamycin complex 1) and Ras/MEK [MAPK (mitogen-activated protein kinase)/ERK (extracellular-signal-regulated kinase) kinase]/ERK pathways for cancer therapy has been pursued for over a decade with limited success. Emerging data have indicated that only discrete subsets of cancer patients have favourable responses to these inhibitors. This is due to genetic mutations that confer drug insensitivity and compensatory mechanisms. Therefore understanding of the feedback mechanisms that occur with respect to specific genetic mutations may aid identification of novel biomarkers that predict patient response. In the present paper, we show that feedback between the PI3K/Akt/mTORC1 and Ras/MEK/ERK pathways is cell-line-specific and highly dependent on the activating mutation of K-Ras or overexpression c-Met. We found that cell lines exhibited differential signalling and apoptotic responses to PD184352, a specific MEK inhibitor, and PI103, a second-generation class I PI3K inhibitor. We reveal that feedback from the PI3K/Akt/mTORC1 to the Ras/MEK/ERK pathway is present in cancer cells harbouring either K-Ras activating mutations or amplification of c-Met but not the wild-type counterparts. Moreover, we demonstrate that inhibition of protein phosphatase activity by OA (okadaic acid) restored PI103-mediated feedback in wild-type cells. Together, our results demonstrate a novel mechanism for feedback between the PI3K/Akt/mTORC1 and the Ras/MEK/ERK pathways that only occurs in K-Ras mutant and c-Met amplified cells but not the isogenic wild-type cells through a mechanism that may involve inhibition of a specific endogenous phosphatase(s) activity. We conclude that monitoring K-Ras and c-Met status are important biomarkers for determining the efficacy of PI103 and other PI3K/Akt inhibitors in cancer therapy.