BackgroundThe proper spatial and temporal regulation of dorsal telencephalic progenitor behavior is a prerequisite for the formation of the highly-organized, six-layered cerebral cortex. Premature differentiation of cells, disruption of cell cycle timing, excessive apoptosis, and/or incorrect neuronal migration signals can have devastating effects, resulting in a number of neurodevelopmental disorders involving microcephaly and/or lissencephaly. Though genes encoding many key players in cortical development have been identified, our understanding remains incomplete. We show that the gene encoding Akirin2, a small nuclear protein, is expressed in the embryonic telencephalon. Converging evidence indicates that Akirin2 acts as a bridge between transcription factors (including Twist and NF-κB proteins) and the BAF (SWI/SNF) chromatin remodeling machinery to regulate patterns of gene expression. Constitutive knockout of Akirin2 is early embryonic lethal in mice, while restricted loss in B cells led to disrupted proliferation and cell survival.MethodsWe generated cortex-restricted Akirin2 knockouts by crossing mice harboring a floxed Akirin2 allele with the Emx1-Cre transgenic line and assessed the resulting embryos using in situ hybridization, EdU labeling, and immunohistochemistry.ResultsThe vast majority of Akirin2 mutants do not survive past birth, and exhibit extreme microcephaly, with little dorsal telencephalic tissue and no recognizable cortex. This is primarily due to massive cell death of early cortical progenitors, which begins at embryonic day (E)10, shortly after Emx1-Cre is active. Immunostaining and cell cycle analysis using EdU labeling indicate that Akirin2-null progenitors fail to proliferate normally, produce fewer neurons, and undergo extensive apoptosis. All of the neurons that are generated in Akirin2 mutants also undergo apoptosis by E12. In situ hybridization for Wnt3a and Wnt-responsive genes suggest defective formation and/or function of the cortical hem in Akirin2 null mice. Furthermore, the apical ventricular surface becomes disrupted, and Sox2-positive progenitors are found to “spill” into the lateral ventricle.ConclusionsOur data demonstrate a previously-unsuspected role for Akirin2 in early cortical development and, given its known nuclear roles, suggest that it may act to regulate gene expression patterns critical for early progenitor cell behavior and cortical neuron production.Electronic supplementary materialThe online version of this article (doi:10.1186/s13064-016-0076-8) contains supplementary material, which is available to authorized users.

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Compared to White women, Latinas are 4 times more likely to contract HIV. In an effort to determine the overall state of the science meant to address this disparity, we reviewed the current HIV prevention intervention literature for U.S. Latinas. We searched 5 online electronic databases from their inception through July, 2014, for HIV prevention interventions including a majority sample of Latinas. Of 1041 articles identified, 20 studies met inclusion criteria. We documented study designs, participant characteristics, outcomes, theories used, and other intervention characteristics. Overall, HIV knowledge and attitudes were the predominant outcome; a small minority of studies included self-reported condom use or STD incidence. Strategies used to address cultural factors specific to Latinas and HIV included; lay health advisors, using ethnographic narratives, or using the Theory of Gender and Power, however few of the interventions adopted these strategies. This study identified several gaps in the intervention literature that need to be addressed. In addition to including more direct measures of decreased HIV risk (ex. condom use), more systematic use of strategies meant to address gender and cultural factors that may place Latinas at increased risk (e.g., gender inequity, traditional gender role norms such as machismo and marianismo, and relationship power dynamics).

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