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The transcriptional regulator Prdm1 is a master gene for the early development of the sensory whisker follicle and is wired to the Lef1 circuitry.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE193357 | GEO | 2022/10/19

REPOSITORIES: GEO

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The transcriptional regulator Prdm1 is a master gene for the early development of the sensory whisker follicle and is wired to the Lef1 circuitry [4C-seq]

Project description:Prdm1 encodes the transcriptional repressor PRDM1/BLIMP1 and Prdm1 mutant mice are one of the rare mutant strains that do not develop whisker hair follicles while still displaying a pelage. We demonstrate that Lef1, a key mediator of the Wnt/Beta Catenin pathway, acts upstream of Prdm1 and identify a primate specific deletion of a Lef1 enhancer, Leaf. This loss may have been significant in the evolutionary process, leading to the progressive defunctionalization and disappearance of vibrissae in primates.

2022-10-19 | GSE193356 | GEO

The transcriptional regulator Prdm1 is a master gene for the early development of the sensory whisker follicle and is wired to the Lef1 circuitry [CUT&TAG]

2022-10-19 | GSE192851 | GEO

The Transcriptional Regulator <i>Prdm1</i> Is Essential for the Early Development of the Sensory Whisker Follicle and Is Linked to the Beta-Catenin First Dermal Signal.

Project description:Prdm1 mutant mice are one of the rare mutant strains that do not develop whisker hair follicles while still displaying a pelage. Here, we show that Prdm1 is expressed at the earliest stage of whisker development in clusters of mesenchymal cells before placode formation. Its conditional knockout in the murine soma leads to the loss of expression of Bmp2, Shh, Bmp4, Krt17, Edar, and Gli1, though leaving the β-catenin-driven first dermal signal intact. Furthermore, we show that Prdm1 expressing cells not only act as a signaling center but also as a multipotent progenitor population contributing to the several lineages of the adult whisker. We confirm by genetic ablation experiments that the absence of macro vibrissae reverberates on the organization of nerve wiring in the mystacial pads and leads to the reorganization of the barrel cortex. We demonstrate that Lef1 acts upstream of Prdm1 and identify a primate-specific deletion of a Lef1 enhancer named Leaf. This loss may have been significant in the evolutionary process, leading to the progressive defunctionalization and disappearance of vibrissae in primates.

| S-EPMC9599752 | biostudies-literature

The transcriptional regulator Prdm1 is a master gene for the early development of the sensory whisker follicle and is wired to the Lef1 circuitry.

Project description:The transcriptional regulator Prdm1 is a master gene for the early development of the sensory whisker follicle and is wired to the Lef1 circuitry.

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The transcriptional regulator Prdm1 is a master gene for the early development of the sensory whisker follicle and is wired to the Lef1 circuitry [CUT&TAG]

Project description:The transcriptional regulator Prdm1 is a master gene for the early development of the sensory whisker follicle and is wired to the Lef1 circuitry [CUT&TAG]

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The transcriptional regulator Prdm1 is a master gene for the early development of the sensory whisker follicle and is wired to the Lef1 circuitry [4C-seq]

Project description:The transcriptional regulator Prdm1 is a master gene for the early development of the sensory whisker follicle and is wired to the Lef1 circuitry [4C-seq]

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Sensory deprivation during early development causes an increased exploratory behavior in a whisker-dependent decision task.

Project description:Stimulation of sensory pathways is important for the normal development of cortical sensory areas, and impairments in the normal development can have long-lasting effect on animal's behavior. In particular, disturbances that occur early in development can cause permanent changes in brain structure and function. The behavioral effect of early sensory deprivation was studied in the mouse whisker system using a protocol to induce a 1-week sensory deprivation immediately after birth. Only two rows of whiskers were spared (C and D rows), and the rest were deprived, to create a situation where an unbalanced sensory input, rather than a complete loss of input, causes a reorganization of the sensory map. Sensory deprivation increased the barrel size ratio of the spared CD rows compared with the deprived AB rows; thus, the map reorganization is likely due, at least in part, to a rewiring of thalamocortical projections. The behavioral effect of such a map reorganization was investigated in the gap-crossing task, where the animals used a whisker that was spared during the sensory deprivation. Animals that had been sensory deprived performed equally well with the control animals in the gap-crossing task, but were more active in exploring the gap area and consequently made more approaches to the gap - approaches that on average were of shorter duration. A restricted sensory deprivation of only some whiskers, although it does not seem to affect the overall performance of the animals, does have an effect on their behavioral strategy on executing the gap-crossing task.

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HDAC3 Is a Master Regulator of mTEC Development.

Project description:The thymus provides a unique microenvironment enabling development and selection of T lymphocytes. Medullary thymic epithelial cells (mTECs) play a pivotal role in this process by facilitating negative selection of self-reactive thymocytes and the generation of Foxp3(+) regulatory T cells. Although studies have highlighted the non-canonical nuclear factor ?B (NF-?B) pathway as the key regulator of mTEC development, comprehensive understanding of the molecular pathways regulating this process still remains incomplete. Here, we demonstrate that the development of functionally competent mTECs is regulated by the histone deacetylase 3 (Hdac3). Although histone deacetylases are global transcriptional regulators, this effect is highly specific only to Hdac3, as neither Hdac1 nor Hdac2 inactivation caused mTEC ablation. Interestingly, Hdac3 induces an mTEC-specific transcriptional program independently of the previously recognized RANK-NF?B signaling pathway. Thus, our findings uncover yet another layer of complexity of TEC lineage divergence and highlight Hdac3 as a major and specific molecular switch crucial for mTEC differentiation.

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FOXN1: A Master Regulator Gene of Thymic Epithelial Development Program.

Project description:T cell ontogeny is a sophisticated process, which takes place within the thymus through a series of well-defined discrete stages. The process requires a proper lympho-stromal interaction. In particular, cortical and medullary thymic epithelial cells (cTECs, mTECs) drive T cell differentiation, education, and selection processes, while the thymocyte-dependent signals allow thymic epithelial cells (TECs) to maturate and provide an appropriate thymic microenvironment. Alterations in genes implicated in thymus organogenesis, including Tbx1, Pax1, Pax3, Pax9, Hoxa3, Eya1, and Six1, affect this well-orchestrated process, leading to disruption of thymic architecture. Of note, in both human and mice, the primordial TECs are yet unable to fully support T cell development and only after the transcriptional activation of the Forkhead-box n1 (FOXN1) gene in the thymic epithelium this essential function is acquired. FOXN1 is a master regulator in the TEC lineage specification in that it down-stream promotes transcription of genes, which, in turn, regulate TECs differentiation. In particular, FOXN1 mainly regulates TEC patterning in the fetal stage and TEC homeostasis in the post-natal thymus. An inborn null mutation in FOXN1 leads to Nude/severe combined immunodeficiency (SCID) phenotype in mouse, rat, and humans. In Foxn1 (-/-) nude animals, initial formation of the primordial organ is arrested and the primordium is not colonized by hematopoietic precursors, causing a severe primary T cell immunodeficiency. In humans, the Nude/SCID phenotype is characterized by congenital alopecia of the scalp, eyebrows, and eyelashes, nail dystrophy, and a severe T cell immunodeficiency, inherited as an autosomal recessive disorder. Aim of this review is to summarize all the scientific information so far available to better characterize the pivotal role of the master regulator FOXN1 transcription factor in the TEC lineage specifications and functionality.

| S-EPMC3709140 | biostudies-literature

MicroRNA398: A Master Regulator of Plant Development and Stress Responses.

Project description:MicroRNAs (miRNAs) play crucial roles in plant development and stress responses, and a growing number of studies suggest that miRNAs are promising targets for crop improvement because they participate in the regulation of diverse, important agronomic traits. MicroRNA398 (miR398) is a conserved miRNA in plants and has been shown to control multiple stress responses and plant growth in a variety of species. There are many studies on the stress response and developmental regulation of miR398. To systematically understand its function, it is necessary to summarize the evolution and functional roles of miR398 and its target genes. In this review, we analyze the evolution of miR398 in plants and outline its involvement in abiotic and biotic stress responses, in growth and development and in model and non-model plants. We summarize recent functional analyses, highlighting the role of miR398 as a master regulator that coordinates growth and diverse responses to environmental factors. We also discuss the potential for fine-tuning miR398 to achieve the goal of simultaneously improving plant growth and stress tolerance.

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