Complex nervous systems have a modular architecture, whereby reiterative groups of neurons ("modules") that share certain structural and functional properties are integrated into large neural circuits. Neurons develop from proliferating progenitor cells that, based on their location and time of appearance, are defined by certain genetic programs. Given that genes expressed by a given progenitor play a fundamental role in determining the properties of its lineage (i.e., the neurons descended from that progenitor), one efficient developmental strategy would be to have lineages give rise to the structural modules of the mature nervous system. It is clear that this strategy plays an important role in neural development of many invertebrate animals, notably insects, where the availability of genetic techniques has made it possible to analyze the precise relationship between neuronal origin and differentiation since several decades. Similar techniques, developed more recently in the vertebrate field, reveal that functional modules of the mammalian cerebral cortex are also likely products of developmentally defined lineages. We will review studies that relate cell lineage to circuitry and function from a comparative developmental perspective, aiming at enhancing our understanding of neural progenitors and their lineages, and translating findings acquired in different model systems into a common conceptual framework.
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http://dx.doi.org/10.1016/j.ydbio.2020.01.012 | DOI Listing |
Commun Biol
December 2024
Fujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, Institute for Basic Medical Sciences, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.
High-fat diet (HFD) induces low-grade chronic inflammation, contributing to obesity and insulin resistance. However, the precise mechanisms triggering obesity-associated metabolic inflammation remain elusive. In this study, we identified epigenetic factor Brd4 as a key player in this process by regulating the expression of Ccr2/Ccr5 in colonic macrophage.
View Article and Find Full Text PDFSci Rep
December 2024
Laboratório de Genética e Evolução Molecular, Universidade Federal do Espírito Santo, Vitória, ES, Brazil.
A recent study proposed a new genetic lineage of leatherback turtles (Dermochelys coriacea) based on genetic analysis, environmental history, and local ecological knowledge (LEK), suggesting the existence of two possible species or subspecies on the beaches of Oaxaca, diverging ~ 13.5 Mya. However, this hypothesis may be influenced by nuclear mitochondrial DNA segments (NUMTs), which could have been misamplified as true mtDNA.
View Article and Find Full Text PDFAdv Sci (Weinh)
December 2024
Department of Cardiology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, 310003, China.
Aortic aneurysm is a life-threatening disease caused by progressive dilation of the aorta and weakened aortic walls. Its pathogenesis involves an imbalance between connective tissue repair and degradation. CD34 cells comprise a heterogeneous population that exhibits stem cell and progenitor cell properties.
View Article and Find Full Text PDFJ Nanobiotechnology
December 2024
State Key Laboratory of Organic-Inorganic Composites, Beijing Laboratory of Biomedical Materials, Beijing University of Chemical Technology, Beijing, 100029, China.
Background: Electrospun nanofiber scaffolds have been widely used in tissue engineering because they can mimic extracellular matrix-like structures and offer advantages including high porosity, large specific surface area, and customizable structure. In this study, we prepared scaffolds composed of aligned and random electrospun polycaprolactone (PCL) nanofibers capable of delivering basic fibroblast growth factor (bFGF) in a sustained manner for repairing damaged tendons.
Results: Aligned and random PCL fiber scaffolds containing bFGF-loaded bovine serum albumin (BSA) nanoparticles (BSA-bFGF NPs, diameter 146 ± 32 nm) were fabricated, respectively.
Trends Biochem Sci
December 2024
Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, VIC 3052, Australia; Department of Medical Biology, University of Melbourne, Parkville, VIC 3052, Australia; Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, VIC 3052, Australia. Electronic address:
Necroptosis is a mode of programmed cell death executed by the mixed lineage kinase domain-like (MLKL) pseudokinase following its activation by the upstream receptor-interacting protein kinase-3 (RIPK3), subsequent to activation of death, Toll-like, and pathogen receptors. The pathway originates in innate immunity, although interest has surged in therapeutically targeting necroptosis owing to its dysregulation in inflammatory diseases. Here, we explore how protein conformation and higher order assembly of the pathway effectors - Z-DNA-binding protein-1 (ZBP1), RIPK1, RIPK3, and MLKL - can be modulated by post-translational modifications, such as phosphorylation, ubiquitylation, and lipidation, and intermolecular interactions to tune activities and modulate necroptotic signaling flux.
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