Publications by authors named "Aracely Castillo Venzor"

Article Synopsis
  • Human germline-soma segregation happens during weeks 2-3 in embryo development, and researchers are studying the specification of primordial germ cells (PGCs) using in vitro models and detailed in vivo datasets.
  • The study reveals a specific molecular signature that indicates a temporary increase in the potential for germ cell development during early epiblast development post-implantation.
  • Additionally, it finds that both PGCs and amniotic cells originate from similar progenitors in the embryo, with TFAP2A being essential for PGC formation, while TFAP2C takes over later in the genetic processes related to PGC fate.
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Article Synopsis
  • - Germline-soma segregation is crucial during mammalian development, and this study focuses on understanding the epigenetic factors involved in human primordial germ cell (hPGC) development using both in vivo models and stem cell techniques that mimic early embryonic stages.
  • - Researchers found that while certain morphogens can temporarily influence mesendoderm development, further activation shifts the focus towards mesoderm and endoderm, with lower levels of the transcription factor OTX2 enhancing the likelihood of hPGC formation.
  • - The study identifies core germline genes regulated by the transcription factors SOX17 and TFAP2C, establishing a network of enhancers crucial for germline development, and highlights the potential of an optimized CR
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Rabbit embryos develop as bilaminar discs at gastrulation as in humans and most other mammals, whereas rodents develop as egg cylinders. Primordial germ cells (PGCs) appear to originate during gastrulation according to many systematic studies on mammalian embryos. Here, we show that rabbit PGC (rbPGC) specification occurs at the posterior epiblast at the onset of gastrulation.

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Altered transcription is a cardinal feature of acute myeloid leukemia (AML); however, exactly how mutations synergize to remodel the epigenetic landscape and rewire three-dimensional DNA topology is unknown. Here, we apply an integrated genomic approach to a murine allelic series that models the two most common mutations in AML: Flt3-ITD and Npm1c. We then deconvolute the contribution of each mutation to alterations of the epigenetic landscape and genome organization, and infer how mutations synergize in the induction of AML.

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The X-chromosomal MECP2/Mecp2 gene encodes methyl-CpG-binding protein 2, a transcriptional activator and repressor regulating many other genes. We discovered in male FVB/N mice that mild (~50%) transgenic overexpression of Mecp2 enhances aggression. Surprisingly, when the same transgene was expressed in C57BL/6N mice, transgenics showed reduced aggression and social interaction.

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