GABAergic interneurons are inhibitory neurons of the nervous system that play a vital role in neural circuitry and activity. They are so named due to their release of the neurotransmitter gamma-aminobutyric acid (GABA), and occupy different areas of the brain. This review will focus primarily on GABAergic interneurons of the mammalian cerebral cortex from a developmental standpoint. There is a diverse amount of cortical interneuronal subtypes that may be categorized by a number of characteristics; this review will classify them largely by the protein markers they express. The developmental origins of GABAergic interneurons will be discussed, as well as factors that influence the complex migration routes that these interneurons must take in order to ultimately localize in the cerebral cortex where they will integrate with the neural circuitry set in place. This review will also place an emphasis on the transcriptional network of genes that play a role in the specification and maintenance of GABAergic interneuron fate. Gaining an understanding of the different aspects of cortical interneuron development and specification, especially in humans, has many useful clinical applications that may serve to treat various neurological disorders linked to alterations in interneuron populations.

SUMMARYOne of the key events in dicot plant embryogenesis is the emergence of the two cotyledon primordia, which marks the transition from radial symmetry to bilateral symmetry. In Arabidopsis thaliana, the three CUP-SHAPED COTYLEDON (CUC) genes are responsible for determining the boundary region between the cotyledons. However, the mechanisms controlling their transcription activation are not well understood. Previous studies found that several WOX family homeobox transcription factors are involved in embryo apical patterning and cotyledon development. Here we show that WOX2 and STIMPY-LIKE (STPL/WOX8) act redundantly to differentially regulate the expression of the CUC genes in promoting the establishment of the cotyledon boundary, without affecting the primary shoot meristem. Loss of both WOX2 and STPL results in reduced CUC2 and CUC3 expression in one side of the embryo, but an expansion of the CUC1 domain. Furthermore, we found that STPL is expressed in the embryo proper, and its activation is enhanced by the removal of WOX2, providing an explanation for the functional redundancy between WOX2 and STPL. Additional evidence also showed that WOX2 and STPL function independently in regulating different aspects of local auxin gradient formation during early embryogenesis.

Asymmetric cell division is a developmental process utilized by several organisms. On the most basic level, an asymmetric division produces two daughter cells, each possessing a different identity or fate. Drosophila melanogaster progenitor cells, referred to as neuroblasts, undergo asymmetric division to produce a daughter neuroblast and another cell known as a ganglion mother cell (GMC). There are several features of asymmetric division in Drosophila that make it a very complex process, and these aspects will be discussed at length. The cell fate determinants that play a role in specifying daughter cell fate, as well as the mechanisms behind setting up cortical polarity within neuroblasts, have proved to be essential to ensuring that neurogenesis occurs properly. The role that mitotic spindle orientation plays in coordinating asymmetric division, as well as how cell cycle regulators influence asymmetric division machinery, will also be addressed. Most significantly, malfunctions during asymmetric cell division have shown to be causally linked with neoplastic growth and tumor formation. Therefore, it is imperative that the developmental repercussions as a result of asymmetric cell division gone awry be understood.