In vertebrates, the female reproductive system arises from the Müllerian (paramesonephric) duct which develops in both sexes under the influence of the Wolffian (mesonephric) duct. For a better understanding of the interactions between the Müllerian duct and its adjacent tissues, we present a systematic scanning and transmission electron microscopic investigation of early stages of avian Müllerian duct development. This starts within the cranial part of the Müllerian ridge from a placode-like thickening and deepening of the coelomic epithelium containing nephrostomes as remnants of the last pronephric and first mesonephric tubules. Groups of cells detach from this placode and rapidly expand caudally as a solid cord. This becomes canalized, but the tip region remains mesenchymal and is found enclosed within the basal lamina of the Wolffian duct. Immunostaining reveals that the Müllerian duct migrates within a matrix rich in laminin and entactin. When the canalized duct has opened into the coelomic cavity, one or more secondary ducts are found immediately caudal of the main funnel, for a short period only, possibly to supply material to the expanding duct. BrdU-anti-BrdU reaction reveals a high proliferation of the duct epithelium. The thickened epithelium of the Müllerian ridge dissolves to form the mesenchymal layers of the duct. Immunostaining with vimentin argues against a cellular contribution of Wolffian duct cells to the Müllerian duct. Comparing the data from avian embryos with those of human indicates that the modalities of early Müllerian duct development are similar in both species.

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MicroRNAs regulate gene expression by destabilizing target mRNA and/or inhibiting translation in animal cells. The ability to mechanistically dissect miR‐124′s function during specification, differentiation, and maturation of neurons during development within a single system has not been accomplished. Using the sea urchin embryo, we take advantage of the manipulability of the embryo and its well‐documented gene regulatory networks (GRNs). We incorporated NeuroD1 as part of the sea urchin neuronal GRN and determined that miR‐124 inhibition resulted in aberrant gut contractions, swimming velocity, and neuronal development. Inhibition of miR‐124 resulted in an increased number of cells expressing transcription factors (TFs) associated with progenitor neurons and a concurrent decrease of mature and functional neurons. Results revealed that in the early blastula/gastrula stages, miR‐124 regulates undefined factors during neuronal specification and differentiation. In the late gastrula/larval stages, miR‐124 regulates Notch and NeuroD1 during the transition between neuronal differentiation and maturation. Overall, we have improved the neuronal GRN and identified miR‐124 to play a prolific role in regulating various transitions of neuronal development.

Neural tube defects are common and serious birth defects in which the brain and/or spinal cord are exposed outside the body. Supplementation of foods with folic acid, an essential vitamin, is linked to a lower risk of neural tube defects; however, the mechanisms by which folic acid influence neural tube defect risk are unclear. Our research seeks to identify the basic cellular roles of known folic acid metabolism genes during morphogenesis using the roundworm Caenorhabditis elegans (C. elegans) as a simple model system. Here, we used live imaging to characterize defects in embryonic development when mel-32 is depleted. mel-32 is an essential folic acid metabolism gene in C. elegans and a homolog to the mammalian enzyme serine hydroxymethyltransferase (Shmt). Disruption of mel-32 resulted in a doubling or tripling of cell cycle lengths and a lack of directed cell movement during embryogenesis. However, the order of cell divisions, as determined by lineage analysis, is unchanged compared to wild type embryos. These results suggest that mel-32/Shmt is required for normal cell cycle lengths in C. elegans.

Mitosis is a fundamental and highly regulated process that acts to faithfully segregate chromosomes into two identical daughter cells. Transcript localization of genes involved in mitosis to the mitotic spindle may be an evolutionarily conserved mechanism to ensure that mitosis occurs in a timely manner. We identified many RNA transcripts that encode proteins involved in mitosis localized at the mitotic spindles in dividing sea urchin embryos and mammalian cells. Disruption of microtubule polymerization, kinesin-1, or dynein results in lack of spindle localization of these transcripts in the sea urchin embryo. Further, results indicate that the cytoplasmic polyadenylation element (CPE) within the 3′UTR of Aurora B, a recognition sequence of CPEB, is essential for RNA localization to the mitotic spindle. Blocking this sequence results in arrested development during early cleavage stages, suggesting that RNA localization to the mitotic spindle may be a regulatory mechanism of cell division that is important for early development.