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The document summarizes research from three different university labs studying neurofascin proteins. A western blot of spinal cords from mice lacking a cerebroside sulfotransferase enzyme showed approximately 35% less neurofascin 155 in the knockout mice compared to controls, while neurofascin 186 and ERK2 levels did not vary. An illustration shows the node of Ranvier in developing and mature neurons, labeling the proteins involved including neurofascin 155 and 186.
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The prevalence of Copy Number Variation (CNV) on human chromosome 16p11.2, identified in approximately 1% of autism spectrum disorder (ASD) cases globally, was found to be 1.2% in an Australian ASD cohort. Bioinformatic analysis identified 13 of the 25 protein coding genes within the 16p11.2 region, including KCTD13, as significantly enriched in the nervous system. Experiments in mice found that suppression of Kctd13 led to impaired radial migration of cortical neurons and altered neuronal morphology, providing insight into how perturbations to KCTD13 expression via 16p11.2 microdeletion could influence brain development. Further experiments showed decreased cell proliferation and mitosis levels
2014 DURF CONFERENCE POSTER
This study investigates a single nucleotide variation (SNV) in the p70 ribosomal S6 kinase 1 (S6K1) gene found in autistic individuals. The researchers introduced the SNV, which changes the amino acid glutamate to glutamine at position 44 (E44Q), into human S6K1 cDNA. When expressed in HEK 293 cells, the mutant S6K1 showed reduced phosphorylation of downstream targets eEF2 and S6 compared to wild-type after insulin stimulation, but did not affect basal protein synthesis levels. Further characterization of this and other S6K1 mutants prevalent in autism could help understand translation control variations linked to the disorder.
2014 DURF CONFERENCE POSTER
This study investigated a single nucleotide variation (SNV) in the p70 ribosomal S6 kinase 1 (S6K1) gene found in autistic individuals. The researchers introduced the SNV, which changes the amino acid glutamate to glutamine at position 44 (E44Q), into human S6K1 cDNA. When expressed in HEK 293 cells, the mutant S6K1 showed reduced phosphorylation of downstream targets eEF2 and S6 compared to wild-type S6K1 following insulin stimulation. However, no difference was found in basal protein synthesis between wild-type and mutant transfected cells. Further studies are needed to better characterize the impact of this S6K1 mutation on protein synthesis and other
Summer Research Poster
The document discusses a study investigating the effects of food restriction on gene expression. It was previously found that 15 genes were upregulated in the brain during food restriction, suggesting they are part of an ancient stress response pathway. The current study aims to test if these genes are also induced in other tissue types under food restriction. Mice were either food restricted or not for 5 days, then gene expression was analyzed using qPCR in various tissues including the kidney. It was found that Angptl4, Mertk, Arrdc2 and Cdkn1a were significantly upregulated in the kidney of food restricted mice compared to controls, providing further evidence they are part of a general stress response pathway activated by food restriction across multiple
Final Poster.
- The study analyzed Alzheimer's disease pathology and expression of the nuclear receptor Nurr1 in 5XFAD mice, a model of severe amyloidosis and neuronal death.
- In the subiculum region of the hippocampus, amyloid plaques and microgliosis increased with age in 5XFAD mice. Significant neuronal loss occurred by 4 months of age.
- Nurr1 expression, which plays a neuroprotective role, decreased in the hippocampus of 5XFAD mice compared to controls by 4 months. Nurr1 was mainly expressed in neurons.
YALE POSTER presentation (3)
- STEP levels are elevated in Fragile X mice and inhibit long-term potentiation.
- Researchers tested the STEP inhibitor TC-2153 in wild type and Fragile X mice.
- TC-2153 treatment led to increased phosphorylation of STEP substrates like NR2B, Pyk2 and ERK1/2 in both wild type and Fragile X mice by inhibiting STEP.
- This suggests that TC-2153 may be an effective treatment for cognitive deficits in Fragile X Syndrome by blocking the elevated STEP activity.
Pandey_et_al-2008-Journal_of_Neurochemistry
1) Rats treated with 3-nitropropionic acid (3-NP), a model of Huntington's disease, exhibited weight loss, gait abnormalities, and striatal lesions.
2) The study found a dose-dependent reduction in complex-I activity in the cerebral cortex of 3-NP treated rats, as measured spectrophotometrically and by blue native-polyacrylamide gel electrophoresis.
3) Succinate driven State 3 respiration was significantly inhibited both in vivo and in isolated mitochondria from the cortex of 3-NP treated rats, suggesting complex-I dysfunction in addition to inhibition of complex-II and succinate dehydrogenase activity contributes to cortico-striatal lesions in this model
Genes,brain & behavior1
1) Mice lacking the inhibitory synapse cell adhesion molecule neuroligin 2 (NL2) were found to exhibit increased anxiety-like behavior.
2) While these NL2-deficient mice appeared to have a decrease in the density of inhibitory synaptic puncta, electron microscopy revealed no actual change in inhibitory synapse numbers.
3) This suggests that NL2 deletion impairs the function of inhibitory synapses without decreasing their numbers, and this decrease in inhibitory synaptic function correlates with increased anxiety in the mice.
PIIS1552526009012771(1)(3)
This document contains summaries of 4 poster presentations from a conference on Alzheimer's disease and dementia research.
The first poster discusses findings that the ER stress transcription factor XBP1s protects against amyloid-beta neurotoxicity in a fruit fly model of Alzheimer's and in human neuroblastoma cells. XBP1s prevents the accumulation of free calcium in the cytosol, explaining its neuroprotective effects.
The second poster reports that amyloid-beta oligomers impair neuronal function and morphology in rat and mouse neuronal cultures and hippocampal slices through a mechanism linked to NMDA receptor signaling and activation of the protein Jacob.
The third poster examines the role of O-GlcNAc glycosylation in hippocampal synaptic
J Neurosci 2006
1) The study demonstrates that phosphorylation of huntingtin protein at serine 421 (S421) protects against toxicity caused by polyglutamine expansion in huntingtin, the cause of Huntington's disease.
2) Calcineurin (CaN), a calcium-activated phosphatase, was found to dephosphorylate S421 both in vitro and in cells. Inhibition of CaN using FK506 increased S421 phosphorylation and prevented polyQ-huntingtin toxicity in neuronal cells.
3) Administration of FK506 to mice also increased phosphorylation of endogenous huntingtin at S421 in the brain. Therefore, inhibition of CaN's dephosphorylation of S421 may have therapeutic potential for treating Huntington's
Ncomms5563
The document reports on a study investigating the molecular mechanisms underlying epilepsy associated with tuberous sclerosis complex (TSC) using a mouse model. The key findings are:
1) Heterozygous Tsc1+/- mice exhibited spontaneous seizures during early postnatal life despite lacking major brain malformations, suggesting haploinsufficiency contributes to the epileptic phenotype.
2) Seizures in Tsc1+/- mice originated in the granular layer (L4) of the neocortex before spreading to other layers.
3) GluN2C-containing NMDA receptors were functionally upregulated in the neocortex of Tsc1+/- mice in an mTOR-dependent manner
Graduate Seminar - Halloween 2009
- The document discusses neuronal cell death in Alzheimer's disease, which is linked to two protein aggregates - amyloid beta plaques and tau tangles. When amyloid beta is introduced to healthy mouse neurons in culture, it leads to rapid cell death.
- Amyloid beta treatment of the neurons increases the activity of calcium-dependent proteases (calpains) and cysteine proteases (caspases), which quickly degrade tau through cleavage into lower molecular weight fragments. This degradation of tau by proteases appears to contribute to neuronal cell death.
- The phosphorylation of tau by kinases such as GSK3 beta and CDK5 also increases after amyloid beta treatment, further implicating tau changes in the neuronal death caused by amyloid
Pre-mRNA splicing and human disease
This document summarizes research on how aberrant pre-mRNA splicing can cause human disease. It notes that 25% of inherited disease-causing mutations affect splicing enhancers and silencers. The study aims to validate mutations in PINK1, a gene associated with Parkinson's disease, that create splicing silencer hexamers and are predicted to disrupt splicing. The researchers will transfect cells with PINK1 reporter constructs containing wild-type or mutant sequences and use RT-PCR and gel electrophoresis to analyze changes in splicing patterns caused by the mutations.
Activity-dependent transcriptional dynamics in mouse primary cortical and hum...
Poster I presented at Lorne Genome 2012. Subsequently formed part of the paper
Barry G, Briggs JA, Vanichkina DP, Poth EM, Beveridge NJ, Ratnu VS, Nayler SP, Nones K, Hu J, Bredy TW, Nakagawa S, Rigo F, Taft RJ, Cairns MJ, Blackshaw S, Wolvetang EJ, Mattick JS (2013). The long non-coding RNA Gomafu is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing. Molecular psychiatry doi: 10.1038/mp.2013.45
Duplicate of http://figshare.com/articles/Activity_dependent_transcriptional_dynamics_in_mouse_primary_cortical_and_human_iPS_derived_neurons/978468
AN_A&D2016
This document summarizes a study examining the relationship between impaired brain insulin signaling, amyloid-beta oligomers (AbOs), tau, and cell cycle reentry (CCR) in Alzheimer's disease (AD) pathogenesis. The study finds that AbOs activate the protein kinase mTORC1, which then phosphorylates tau and induces CCR in neurons. CCR can be prevented by insulin-stimulated activation of lysosomal mTORC1. As AbOs also reduce neuronal insulin signaling, decreased insulin signaling allows the toxic effects of AbOs to cause CCR and neuronal death, contributing to AD progression. The findings help explain how impaired brain insulin signaling may promote AD by unleashing the cell cycle reentry effects of Ab
Similar to Lab Photo History (20)
Temporal-Spatial Expressions of Spy1 in Rat Sciatic Nerve After Crush
Temporal-Spatial Expressions of Spy1 in Rat Sciatic Nerve After Crush
Activity-dependent transcriptional dynamics in mouse primary cortical and hum...
Activity-dependent transcriptional dynamics in mouse primary cortical and hum...
Lab Photo History
- 1. Michael Deininger's Lab, The University of Utah - 2011
- 2. Jeff Dupree's Lab, Virginia Commonwealth University - 2008
- 3. Kelli Hoover's Lab, The Pennsylvania State University - 2002
- 4. Western blot of spinal cords from 15 day old mice shows that there is ~35% less neurofascin 155 (Nfasc155, oligodendrocyte-specific) in the cerebroside sulfotransferase knockout (KO) mice. Neurofascin 186 (Nfasc186, neuron-specific) and extracellular-regulated kinase 2 (ERK2, loading control) do not vary. n≥3, p=0.001 Adapted from Pomicter et al ., Brain 2010:133;389-405.
- 5. A developing (left) and mature (right) node:paranode (blue:orange) region is shown with voltage-gated sodium channels in blue, contactin-associated protein in red, and neurofascin proteins (186 at the neuronal node and 155 at the myelin paranode) in green. Bar = 5 μ m. Adapted from Pomicter et al ., Brain 2010:133;389-405.