Planar cell polarity zebrafish models of congenital scoliosis reveal underlying defects in notochord morphogenesis.

Congenital scoliosis (CS) is a type of vertebral malformation for which the etiology remains elusive. The notochord is pivotal for vertebrae development, but its role in CS is still understudied. Here, we generated a zebrafish knockout of ptk7a, a planar cell polarity (PCP) gene that is essential for convergence and extension (C&E) of the notochord, and detected congenital scoliosis-like vertebral malformations (CVMs).

The risk of contact between visitors and Borrelia burgdorferi-infected ticks is associated with fine-scale landscape features in a southeastern Canadian nature park.

Background: Infectious diseases are emerging across temperate regions of the world, and, for some, links have been made between landscapes and emergence dynamics. For tick-borne diseases, public parks may be important exposure sites for people living in urbanized areas of North America and Europe. In most cases, we know more about the ecological processes that determine the hazard posed by ticks as disease vectors than we do about how human population exposure varies in urban natural parks.

Site occupancy by American martens and fishers in temperate deciduous forests of Québec.

Interspecific interactions can mediate site occupancy of sympatric species and can be a key factor in habitat use patterns. American martens () and Fishers ( are two sympatric mesocarnivores in eastern North American forests. Due to their larger size, fishers have a competitive advantage over martens.

Lowering the rate of timber harvesting to mitigate impacts of climate change on boreal caribou habitat quality in eastern Canada.

Many boreal populations of woodland caribou (Rangifer tarandus caribou) have declined in Canada, a trend essentially driven by the increasing footprint of anthropogenic disturbances and the resulting habitat-mediated apparent competition that increases predation pressure. However, the influence of climate change on these ecological processes remains poorly understood. We evaluated how climate change will affect boreal caribou habitat over the 2030-2100 horizon and in a 9.

Interpericyte tunnelling nanotubes regulate neurovascular coupling.

Signalling between cells of the neurovascular unit, or neurovascular coupling, is essential to match local blood flow with neuronal activity. Pericytes interact with endothelial cells and extend processes that wrap capillaries, covering up to 90% of their surface area. Pericytes are candidates to regulate microcirculatory blood flow because they are strategically positioned along capillaries, contain contractile proteins and respond rapidly to neuronal stimulation, but whether they synchronize microvascular dynamics and neurovascular coupling within a capillary network was unknown.

The Novel Small Molecule TRVA242 Stabilizes Neuromuscular Junction Defects in Multiple Animal Models of Amyotrophic Lateral Sclerosis.

Amyotrophic lateral sclerosis (ALS) is a debilitating neurodegenerative disorder in which the neuromuscular junction progressively degenerates, leading to movement difficulties, paralysis, and eventually death. ALS is currently being treated by only two FDA-approved drugs with modest efficacy in slowing disease progression. Often, the translation of preclinical findings to bedside terminates prematurely as the evaluation of potential therapeutic compounds focuses on a single study or a single animal model.

Corrigendum: The Dietary Flavonoid, Luteolin, Negatively Affects Neuronal Differentiation.

[This corrects the article DOI: 10.3389/fnmol.2019.

secCl is a cys-loop ion channel necessary for the chloride conductance that mediates hormone-induced fluid secretion in Drosophila.

Organisms use circulating diuretic hormones to control water balance (osmolarity), thereby avoiding dehydration and managing excretion of waste products. The hormones act through G-protein-coupled receptors to activate second messenger systems that in turn control the permeability of secretory epithelia to ions like chloride. In insects, the chloride channel mediating the effects of diuretic hormones was unknown.

Individual knock out of glycine receptor alpha subunits identifies a specific requirement of glra1 for motor function in zebrafish.

Glycine receptors (GlyRs) are ligand-gated chloride channels mediating inhibitory neurotransmission in the brain stem and spinal cord. They function as pentamers composed of alpha and beta subunits for which 5 genes have been identified in human (GLRA1, GLRA2, GLRA3, GLRA4, GLRB). Several in vitro studies showed that the pentameric subtype composition as well as its stoichiometry influence the distribution and the molecular function of the receptor.

Single and Synergistic Effects of Cannabidiol and Δ-9-Tetrahydrocannabinol on Zebrafish Models of Neuro-Hyperactivity.

In this study, we aimed to investigate the effect of the two main active cannabinoids extracted from cannabis: Δ-9-tetrahydrocannabinol (THC) and cannabidiol (CBD) on two distinct behavioral models of induced neuro-hyperactivity. We have taken advantage of two previously developed zebrafish models of neuro-hyperactivity: a chemically induced pentylenetetrazole model and a genetic model caused by loss-of-function mutations in the GABA receptor subunit alpha 1 (). Both CBD and THC have a significant effect on the behavioral changes induced by both models.

The Dietary Flavonoid, Luteolin, Negatively Affects Neuronal Differentiation.

Luteolin, a polyphenolic plant flavonoid, has been attributed with numerous beneficial properties like anti-cancer, antioxidant, and anti-inflammatory action. Luteolin has been reported earlier to be neuroprotective in models of spinal cord injury and traumatic brain injury and also induces neurite outgrowth in PC12 cells. However, the effect of luteolin on early differentiation, which might be important for its beneficial effects, is unknown.

Glycine Regulates Neural Stem Cell Proliferation During Development Lnx1-Dependent Notch Signaling.

During development of the zebrafish embryo, glycine signaling promotes the differentiation of neural stem cells (NSCs). We found that glycine signaling suppresses the expression of Ligand of Numb X1 (, Ligand of numb protein-x1), a gene of unknown function during NSC differentiation that is selectively expressed in the embryonic central nervous system (CNS). As a consequence, Numb levels were stabilized and Notch activity (measured as expression) was reduced, promoting NSC differentiation.

Transcriptomic Analysis of Zebrafish TDP-43 Transgenic Lines.

Amyotrophic lateral sclerosis (ALS) is a late-onset progressive neurodegenerative disorder that affects both upper and lower motor neurons, leading to muscle atrophy with spasticity and eventual death in 3-5 years after the disease onset. More than 50 mutations linked to ALS have been found in the gene , encoding the protein TDP-43 that is the predominant component of neuronal inclusions in ALS. TDP-43 is an RNA binding protein with glycine-rich domains that binds to more than 6,000 RNAs in the human brain.

Neuromuscular junction abnormalities in a zebrafish loss-of-function model of TDP-43.

Almost 90% of amyotrophic lateral sclerosis (ALS) cases are characterized by the presence of aggregates of insoluble, misfolded cytoplasmic TAR DNA binding protein of 43 kDa (TDP-43). Distal axonopathy with impaired neuromuscular junctions (NMJs) before motor neuron degeneration or clinical onset of symptoms has been hypothesized as an early pathology in ALS. However, synaptic defects at the NMJ caused by TDP-43 mutations have not been characterized.

Glycine decarboxylase deficiency-induced motor dysfunction in zebrafish is rescued by counterbalancing glycine synaptic level.

Glycine encephalopathy (GE), or nonketotic hyperglycinemia (NKH), is a rare recessive genetic disease caused by defective glycine cleavage and characterized by increased accumulation of glycine in all tissues. Here, based on new case reports of GLDC loss-of-function mutations in GE patients, we aimed to generate a zebrafish model of severe GE in order to unravel the molecular mechanism of the disease. Using CRISPR/Cas9, we knocked out the gldc gene and showed that gldc-/- fish recapitulate GE on a molecular level and present a motor phenotype reminiscent of severe GE symptoms.

Hindcasting the impacts of land-use changes on bird communities with species distribution models of Bird Atlas data.

Habitat loss and degradation induced by human development are among the major threats to biodiversity worldwide. In this study, we tested our ability to predict the response of bird communities (128 species) to land-use changes in southern Quebec (~483,100 km ) over the last 30 yr (between 1984-1989 and 2010-2014) by using species distribution models (299,302 occurrences in 30,408 locations) from a hindcasting perspective. Results were grouped by functional guilds to infer potential impacts on ecosystem services, and to relate model transferability (i.

Glycine Promotes the Survival of a Subpopulation of Neural Stem Cells.

Glycine is mainly known as an inhibitory neurotransmitter in adult mature neurons, regulating neuronal network activity in the central nervous system. In contrast, during embryogenesis glycine can act as an excitatory neurotransmitter and generates the first electrical signal in immature neurons. The roles and functional significance of this excitatory glycinergic activity during neurodevelopment are still unclear.

The positive carbon stocks-biodiversity relationship in forests: co-occurrence and drivers across five subclimates.

Carbon storage in forests and its ability to offset global greenhouse gas emissions, as well as biodiversity and its capacity to support ecosystem functions and services, are often considered separately in landscape planning. However, the potential synergies between them are currently poorly understood. Identifying the spatial patterns and factors driving their co-occurrence across different climatic zones is critical to more effectively conserve forest ecosystems at the regional level.

Non-canonical mTOR-Independent Role of DEPDC5 in Regulating GABAergic Network Development.

Mutations in DEPDC5 are causal factors for a broad spectrum of focal epilepsies, but the underlying pathogenic mechanisms are still largely unknown. To address this question, a zebrafish depdc5 knockout model showing spontaneous epileptiform events in the brain, increased drug-induced seizure susceptibility, general hypoactivity, premature death at 2-3 weeks post-fertilization, as well as the expected hyperactivation of mTOR signaling was developed. Using this model, the role of DEPDC5 in brain development was investigated using an unbiased whole-transcriptomic approach.

RNA-Sequencing Reveals Unique Transcriptional Signatures of Running and Running-Independent Environmental Enrichment in the Adult Mouse Dentate Gyrus.

Environmental enrichment (EE) is a powerful stimulus of brain plasticity and is among the most accessible treatment options for brain disease. In rodents, EE is modeled using multi-factorial environments that include running, social interactions, and/or complex surroundings. Here, we show that running and running-independent EE differentially affect the hippocampal dentate gyrus (DG), a brain region critical for learning and memory.

Expression of C9orf72-related dipeptides impairs motor function in a vertebrate model.

Large expansions of hexanucleotide GGGGCC (G4C2) repeats (hundreds to thousands) in the first intron of the chromosome 9 open reading frame 72 (C9orf72) locus are the strongest known genetic factor associated with amyotrophic lateral sclerosis and frontotemporal lobar degeneration. Different hypotheses exist about the underlying disease mechanism including loss of function by haploinsufficiency, toxicity arising as a result of RNA or dipeptide repeats (DPRs). Five different DPRs are produced by repeat-associated non-ATG-initiated translation of the G4C2 repeats.

Neuroleptics as therapeutic compounds stabilizing neuromuscular transmission in amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a rapidly progressing, fatal disorder with no effective treatment. We used simple genetic models of ALS to screen phenotypically for potential therapeutic compounds. We screened libraries of compounds in C.