Homologous chromosome pairing is a prerequisite to establish physical linkage between homologs, which is critical for faithful chromosome segregation during meiosis I. The establishment of pairing is genetically separable from subsequent synapsis, defined as stabilization of pairing by the synaptonemal complex (SC). The underlying mechanism of presynaptic pairing is poorly understood. In the nematode Caenorhabditis elegans, a unique cis-acting element, the pairing center (PC), is essential for presynaptic pairing; however, it is not known whether and how the remainder of the chromosome contributes to presynaptic pairing. Here we report direct evidence for presynaptic pairing activity intrinsic to non-PC regions, which is facilitated by a conserved chromodomain protein, MRG-1. In mrg-1 loss-of-function mutants, pairing is compromised specifically in non-PC regions, leading to nonhomologous SC assembly. Our data support a model in which presynaptic alignment in non-PC regions collaborates with initial PC pairing to ensure correct homologous synapsis.
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http://dx.doi.org/10.1016/j.devcel.2011.09.019 | DOI Listing |
Nano Converg
January 2025
Bendable Electronics and Sustainable Technologies (BEST) Group, Electrical and Computer Engineering Department, Northeastern University, Boston, MA, 02115, USA.
The intriguing way the receptors in biological skin encode the tactile data has inspired the development of electronic skins (e-skin) with brain-inspired or neuromorphic computing. Starting with local (near sensor) data processing, there is an inherent mechanism in play that helps to scale down the data. This is particularly attractive when one considers the huge data produced by large number of sensors expected in a large area e-skin such as the whole-body skin of a robot.
View Article and Find Full Text PDFActa Physiol (Oxf)
February 2025
Institute for Physiology, University Medical Centre of the Johannes Gutenberg University Mainz, Mainz, Germany.
Aim: Despite dysfunctional vasoactive intestinal polypeptide-positive interneurons (VIP-INs) being linked to the emergence of neurodevelopmental disorders, the temporal profile of VIP-IN functional maturation and cortical network integration remains unclear.
Methods: Postnatal VIP-IN development was traced with patch clamp experiments in the somatosensory cortex of Vip-IRES-cre x tdTomato mice. Age groups were chosen during barrel field formation, before and after activation of main sensory inputs, and in adult animals (postnatal days (P) P3-4, P8-10, P14-16, and P30-36).
bioRxiv
December 2024
Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Fluorescent reporters for glutamate release and postsynaptic Ca signaling are essential tools for quantifying synapse functional heterogeneity across neurons and circuits. However, leveraging these probes for neuroscience requires scalable experimental frameworks. Here, we devised a high-throughput approach to efficiently collect and analyze hundreds of optical recordings of glutamate release activity at presynaptic boutons in cultured rat hippocampal neurons.
View Article and Find Full Text PDFElife
December 2024
Auditory Neuroscience and Synaptic Nanophysiology Group, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany.
Neural diversity can expand the encoding capacity of a circuitry. A striking example of diverse structure and function is presented by the afferent synapses between inner hair cells (IHCs) and spiral ganglion neurons (SGNs) in the cochlea. Presynaptic active zones at the pillar IHC side activate at lower IHC potentials than those of the modiolar side that have more presynaptic Ca channels.
View Article and Find Full Text PDFBrain Res Bull
January 2025
School of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK.
The negative interference of treatments between the acetylcholinesterase inhibitor rivastigmine and the tau aggregation inhibitor hydromethylthionine mesylate (HMTM) has been reported in Line 1 tau-transgenic mice, which overexpress a truncated species of tau protein that is found in the core of paired helical filaments in Alzheimer´s disease (AD). However, little is known about whether such interactions could affect synapses in mice overexpressing tau carrying pathogenic mutations. Here, we have used Line 66 (L66) mice which overexpress full-length human tau carrying the P301S mutation as a model in which tau accumulates in synapses.
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