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Korb E, Herre M, Zucker-Scharff I, Darnell RB, Allis CD
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BET protein Brd4 activates transcription in neurons and BET inhibitor Jq1 blocks memory in mice
NATURE NEUROSCIENCE 2015 OCT; 18(10):1464-1473
Precise regulation of transcription is crucial for the cellular mechanisms underlying memory formation. However, the link between neuronal stimulation and the proteins that directly interact with histone modifications to activate transcription in neurons remains unclear. Brd4 is a member of the bromodomain and extra-terminal domain ( BET) protein family, which binds acetylated histones and is a critical regulator of transcription in many cell types, including transcription in response to external cues. Small molecule BET inhibitors are in clinical trials, yet almost nothing is known about Brd4 function in the brain. Here we show that Brd4 mediates the transcriptional regulation underlying learning and memory. The loss of Brd4 function affects critical synaptic proteins, which results in memory deficits in mice but also decreases seizure susceptibility. Thus Brd4 provides a critical link between neuronal activation and the transcriptional responses that occur during memory formation.
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Search for supersymmetry with photons in pp collisions at root s=8 TeV
PHYSICAL REVIEW D 2015 OCT 19; 92(7):? Article 072006
Two searches for physics beyond the standard model in events containing photons are presented. The data sample used corresponds to an integrated luminosity of 19.7 fb(-1) of proton-proton collisions at root s = 8 TeV, collected with the CMS experiment at the CERN LHC. The analyses pursue different inclusive search strategies. One analysis requires at least one photon, at least two jets, and a large amount of transverse momentum imbalance, while the other selects events with at least two photons and at least one jet, and uses the razor variables to search for signal events. The background expected from standard model processes is evaluated mainly from data. The results are interpreted in the context of general gauge-mediated supersymmetry, with the next-to-lightest supersymmetric particle either a bino- or wino-like neutralino, and within simplified model scenarios. Upper limits at the 95% confidence level are obtained for cross sections as functions of the masses of the intermediate supersymmetric particles.
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Search for a Higgs boson in the mass range from 145 to 1000 GeV decaying to a pair of W or Z bosons
JOURNAL OF HIGH ENERGY PHYSICS 2015 OCT 22; ?(10):? Article 144
A search for a heavy Higgs boson in the H -> WW and H -> ZZ decay channels is reported. The search is based upon proton-proton collision data samples corresponding to an integrated luminosity of up to 5.1 fb(-1) at root s = 7 TeV and up to 19.7 fb(-1) at root s = 8 TeV, recorded by the CMS experiment at the CERN LHC. Several final states of the H -> WW and H -> ZZ decays are analyzed. The combined upper limit at the 95% confidence level on the product of the cross section and branching fraction exclude a Higgs boson with standard model-like couplings and decays in the range 145 < m(H) < 1000 GeV. We also interpret the results in the context of an electroweak singlet extension of the standard model.
Ma Q, Yang JM, Li T, Milner TA, Hempstead BL
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Selective reduction of striatal mature BDNF without induction of proBDNF in the zQ175 mouse model of Huntington's disease
NEUROBIOLOGY OF DISEASE 2015 OCT; 82(?):466-477
Huntington's disease (HD) is a neurodegenerative disorder characterized by massive loss of medium spiny neurons in the striatum. However, the mechanisms by which mutant huntingtin leads to this selective neuronal death remain incompletely understood. Brain-derived neurotrophic factor (BDNF) has been shown to be neuroprotective on HD striatal neurons both in vitro and in vivo. ProBDNF, the precursor of mature BDNF (mBDNF), also can be secreted but promotes apoptosis of neurons expressing p75(NTR) and sortilin receptors. Although a reduction of total striatal BDNF protein has been reported in HD patients and mouse models, it remains unclear whether conversion of proBDNF to mBDNF is altered in HD, and whether the proBDNF receptors, p75(NTR) and sortilin are dysregulated, leading to impaired striatal neuron survival. To test these hypotheses, we generated bdnf-HA knock-in (MI) mice on the zQ175 HD background to accurately quantitate the levels of both proBDNF and mBDNF in the HD striatum. In aged zQ175 HD mice, we observed a significant loss of mBDNF and decreased TrkB activation, but no increase of proBDNF or p75(NTR) levels either in the sensorimotor cortex or the striatum cortilin receptor are both increased in immature striatal oligodenHD striatum. Taken together, the present study through the TrkB receptor, rather than an induction factor to the vulnerability of striatal neurons in the zQ175 HD mouse model. (C) 2015 Elsevier Inc All rights reserved.
Marraffini LA
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CRISPR-Cas immunity in prokaryotes
NATURE 2015 OCT 1; 526(7571):55-61
Prokaryotic organisms are threatened by a large array of viruses and have developed numerous defence strategies. Among these, only clustered, regularly interspaced short palindromic repeat (CRISPR)-Cas systems provide adaptive immunity against foreign elements. Upon viral injection, a small sequence of the viral genome, known as a spacer, is integrated into the CRISPR locus to immunize the host cell. Spacers are transcribed into small RNA guides that direct the cleavage of the viral DNA by Cas nucleases. Immunization through spacer acquisition enables a unique form of evolution whereby a population not only rapidly acquires resistance to its predators but also passes this resistance mechanism vertically to its progeny.
Sathyanesan M, Girgenti MJ, Warner-Schmidt J, Newton SS
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Indomethacin induced gene regulation in the rat hippocampus
MOLECULAR BRAIN 2015 OCT 6; 8(?):? Article 59
Background: Non-steroidal anti-inflammatory drugs such as indomethacin are widely used to treat inflammatory diseases and manage pain, fever and inflammation in several conditions, including neuropsychiatric disorders. Although they predominantly function by inhibiting cyclooxygenase (COX) activity, important COX-independent actions also occur. These actions could be responsible for the adverse side effects associated with chronic and/or high dose usage of this popular drug class. Results: We examined gene regulation in the hippocampus after peripheral administration of indomethacin by employing a microarray approach. Secondary confirmation and the brain expression pattern of regulated genes was examined by in situ hybridization and immunohistochemistry. Transglutaminase 2, serum glucocorticoid inducible kinase, Inhibitor of NF-kappa B and vascular endothelial growth factor were among genes that were prominently upregulated, while G-protein coupled receptor 56 and neuropeptide Y were among genes that were downregulated by indomethacin. Co-localization studies using blood vessel markers revealed that transglutaminase 2 was induced specifically in brain vasculature. Conclusions: The data demonstrate that COX-inhibitors can differentially regulate gene transcription in multiple, functionally distinctly cell types in the brain. The results provide additional insight into the molecular actions of COX-inhibitors and indicate that their effects on vasculature could influence cerebral blood flow mechanisms.
Wheeler DB, Zoncu R, Root DE, Sabatini DM, Sawyers CL
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Identification of an oncogenic RAB protein
SCIENCE 2015 OCT 9; 350(6257):211-217
In a short hairpin RNA screen for genes that affect AKT phosphorylation, we identified the RAB35 small guanosine triphosphatase (GTPase)-a protein previously implicated in endomembrane trafficking-as a regulator of the phosphatidylinositol 3'-OH kinase (PI3K) pathway. Depletion of RAB35 suppresses AKT phosphorylation in response to growth factors, whereas expression of a dominant active GTPase-deficient mutant of RAB35 constitutively activates the PI3K/AKT pathway. RAB35 functions downstream of growth factor receptors and upstream of PDK1 and mTORC2 and copurifies with PI3K in immunoprecipitation assays. Two somatic RAB35 mutations found in human tumors generate alleles that constitutively activate PI3K/AKT signaling, suppress apoptosis, and transform cells in a PI3K-dependent manner. Furthermore, oncogenic RAB35 is sufficient to drive platelet-derived growth factor receptor a to LAMP2-positive endomembranes in the absence of ligand, suggesting that there may be latent oncogenic potential in dysregulated endomembrane trafficking.
Huang TT, Lai HC, Ko YF, Ojcius DM, Lan YW, Martel J, Young JD, Chong KY
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Hirsutella sinensis mycelium attenuates bleomycin-induced pulmonary inflammation and fibrosis in vivo
SCIENTIFIC REPORTS 2015 OCT 26; 5(?):? Article 15282
Hirsutella sinensis mycelium (HSM), the anamorph of Cordyceps sinensis, is a traditional Chinese medicine that has been shown to possess various pharmacological properties. We previously reported that this fungus suppresses interleukin-1 beta and IL-18 secretion by inhibiting both canonical and non-canonical inflammasomes in human macrophages. However, whether HSM may be used to prevent lung fibrosis and the mechanism underlying this activity remain unclear. Our results show that pretreatment with HSM inhibits TGF-beta 1-induced expression of fibronectin and alpha-SMA in lung fibroblasts. HSM also restores superoxide dismutase expression in TGF-beta 1-treated lung fibroblasts and inhibits reactive oxygen species production in lung epithelial cells. Furthermore, HSM pretreatment markedly reduces bleomycin-induced lung injury and fibrosis in mice. Accordingly, HSM reduces inflammatory cell accumulation in bronchoalveolar lavage fluid and proinflammatory cytokines levels in lung tissues. The HSM extract also significantly reduces TGF-beta 1 in lung tissues, and this effect is accompanied by decreased collagen 3 alpha 1 and alpha-SMA levels. Moreover, HSM reduces expression of the NLRP3 inflammasome and P2X(7)R in lung tissues, whereas it enhances expression of superoxide dismutase. These findings suggest that HSM may be used for the treatment of pulmonary inflammation and fibrosis.
Rueger S, Bochud PY, Dufour JF, Mullhaupt B, Semela D, Heim MH, Moradpour D, Cerny A, Malinverni R, Booth DR, Suppiah V, George J, Argiro L, Halfon P, Bourliere M, Talal AH, Jacobson IM, Patin E, Nalpas B, Poynard T, Pol S, Abel L, Kutalik Z, Negro F
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Impact of common risk factors of fibrosis progression in chronic hepatitis C
GUT 2015 OCT; 64(10):1605-1615
Objective The natural course of chronic hepatitis C varies widely. To improve the profiling of patients at risk of developing advanced liver disease, we assessed the relative contribution of factors for liver fibrosis progression in hepatitis C. Design We analysed 1461 patients with chronic hepatitis C with an estimated date of infection and at least one liver biopsy. Risk factors for accelerated fibrosis progression rate (FPR), defined as >= 0.13 Metavir fibrosis units per year, were identified by logistic regression. Examined factors included age at infection, sex, route of infection, HCV genotype, body mass index (BMI), significant alcohol drinking (>= 20 g/day for >= 5 years), HIV coinfection and diabetes. In a subgroup of 575 patients, we assessed the impact of single nucleotide polymorphisms previously associated with fibrosis progression in genome-wide association studies. Results were expressed as attributable fraction (AF) of risk for accelerated FPR. Results Age at infection (AF 28.7%), sex (AF 8.2%), route of infection (AF 16.5%) and HCV genotype (AF 7.9%) contributed to accelerated FPR in the Swiss Hepatitis C Cohort Study, whereas significant alcohol drinking, anti-HIV, diabetes and BMI did not. In genotyped patients, variants at rs9380516 (TULP1), rs738409 (PNPLA3), rs4374383 (MERTK) (AF 19.2%) and rs910049 (major histocompatibility complex region) significantly added to the risk of accelerated FPR. Results were replicated in three additional independent cohorts, and a meta-analysis confirmed the role of age at infection, sex, route of infection, HCV genotype, rs738409, rs4374383 and rs910049 in accelerating FPR. Conclusions Most factors accelerating liver fibrosis progression in chronic hepatitis C are unmodifiable.
Heller E, Fuchs E
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Tissue patterning and cellular mechanics
JOURNAL OF CELL BIOLOGY 2015 OCT 26; 211(2):219-231
In development, cells organize into biological tissues through cell growth, migration, and differentiation. Globally, this process is dictated by a genetically encoded program in which secreted morphogens and cell-cell interactions prompt the adoption of unique cell fates. Yet, at its lowest level, development is achieved through the modification of cell cell adhesion and actomyosin-based contractility, which set the level of tension within cells and dictate how they pack together into tissues. The regulation of tension within individual cells and across large groups of cells is a major driving force of tissue organization and the basis of all cell shape change and cell movement in development.