In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.

Ex Input:
The Snail transcription factor plays a key role in regulating diverse developmental processes but is not thought to play a role in mammalian neural precursors. Here, we have examined radial glial precursor cells of the embryonic murine cortex and demonstrate that Snail regulates their survival, self-renewal, and differentiation into intermediate progenitors and neurons via two distinct and separable target pathways. First, Snail promotes cell survival by antagonizing a p53-dependent death pathway because coincident p53 knockdown rescues survival deficits caused by Snail knockdown. Second, we show that the cell cycle phosphatase Cdc25b is regulated by Snail in radial precursors and that Cdc25b coexpression is sufficient to rescue the decreased radial precursor proliferation and differentiation observed upon Snail knockdown. Thus, Snail acts via p53 and Cdc25b to coordinately regulate multiple aspects of mammalian embryonic neural precursor biology.

Ex Output:
Snail coordinately regulates downstream pathways to control multiple aspects of mammalian neural precursor development.

Ex Input:
CD8(+) T cells can respond to unrelated infections in an Ag-independent manner. This rapid innate-like immune response allows Ag-experienced T cells to alert other immune cell types to pathogenic intruders. In this study, we show that murine CD8(+) T cells can sense TLR2 and TLR7 ligands, resulting in rapid production of IFN- but not of TNF- and IL-2. Importantly, Ag-experienced T cells activated by TLR ligands produce sufficient IFN- to augment the activation of macrophages. In contrast to Ag-specific reactivation, TLR-dependent production of IFN- by CD8(+) T cells relies exclusively on newly synthesized transcripts without inducing mRNA stability. Furthermore, transcription of IFN- upon TLR triggering depends on the activation of PI3K and serine-threonine kinase Akt, and protein synthesis relies on the activation of the mechanistic target of rapamycin. We next investigated which energy source drives the TLR-induced production of IFN-. Although Ag-specific cytokine production requires a glycolytic switch for optimal cytokine release, glucose availability does not alter the rate of IFN- production upon TLR-mediated activation. Rather, mitochondrial respiration provides sufficient energy for TLR-induced IFN- production. To our knowledge, this is the first report describing that TLR-mediated bystander activation elicits a helper phenotype of CD8(+) T cells. It induces a short boost of IFN- production that leads to a significant but limited activation of Ag-experienced CD8(+) T cells. This activation suffices to prime macrophages but keeps T cell responses limited to unrelated infections.

Ex Output:
TLR-Mediated Innate Production of IFN- by CD8+ T Cells Is Independent of Glycolysis.

Ex Input:
Planar cell polarity (PCP) is observed in an array of developmental processes that involve collective cell movement and tissue organization, and its disruption can lead to severe developmental defects. Recent studies in flies and vertebrates have identified new functions for PCP as well as new signalling components, and have proposed new mechanistic models. However, despite this progress, the search to simplify principles of understanding continues and important mechanistic uncertainties still pose formidable challenges.

Ex Output:
Pointing in the right direction: new developments in the field of planar cell polarity