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Leibowitz SF
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Introduction to special issue of Physiology and Behavior: A tribute to Bart Hoebel
PHYSIOLOGY & BEHAVIOR 2011 JUL 25; 104(1):1-3
Darnell JC, Van Driesche SJ, Zhang CL, Hung KYS, Mele A, Fraser CE, Stone EF, Chen C, Fak JJ, Chi SW, Licatalosi DD, Richter JD, Darnell RB
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FMRP Stalls Ribosomal Translocation on mRNAs Linked to Synaptic Function and Autism
CELL 2011 JUL 22; 146(2):247-261
FMRP loss of function causes Fragile X syndrome (FXS) and autistic features. FMRP is a polyribosome-associated neuronal RNA-binding protein, suggesting that it plays a key role in regulating neuronal translation, but there has been little consensus regarding either its RNA targets or mechanism of action. Here, we use high-throughput sequencing of RNAs isolated by crosslinking immunoprecipitation (HITS-CLIP) to identify FMRP interactions with mouse brain polyribosomal mRNAs. FMRP interacts with the coding region of transcripts encoding pre- and postsynaptic proteins and transcripts implicated in autism spectrum disorders (ASD). We developed a brain polyribosome-programmed translation system, revealing that FMRP reversibly stalls ribosomes specifically on its target mRNAs. Our results suggest that loss of a translational brake on the synthesis of a subset of synaptic proteins contributes to FXS. In addition, they provide insight into the molecular basis of the cognitive and allied defects in FXS and ASD and suggest multiple targets for clinical intervention.
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Walsh S, Zaganidis N, Basegmez S, Bruno G, Caudron J, Ceard L, Gil EC, De Jeneret JD, Delaere C, Favart D, Giammanco A, Gregoire G, Hollar J, Lemaitre V, Liao J, Militaru O, Nuttens C, Ovyn S, Pagano D, Pin A, Piotrzkowski K, Schul N, Beliy N, Caebergs T, Daubie E, Alves GA, Brito L, Damiao DD, Pol ME, Souza MHG, Alda WL, Carvalho W, Da Costa EM, Martins CD, De Souza SF, Mundim L, Nogima H, Oguri V, Da Silva WLP, Santoro A, Do Amaral SMS, Sznajder A, Bernardes CA, Dias FA, Tomei TRFP, Gregores EM, Lagana C, Marinho F, Mercadante PG, Novaes SF, Padula SS, Darmenov N, Genchev V, Iaydjiev P, Piperov S, Rodozov M, Stoykova S, Sultanov G, Tcholakov V, Trayanov R, Dimitrov A, Hadjiiska R, Karadzhinova A, Kozhuharov V, Litov L, Mateev M, Pavlov B, Petkov P, Bian JG, Chen GM, Chen HS, Jiang CH, Liang D, Liang S, Meng X, Tao J, Wang J, Wang J, Wang X, Wang Z, Xiao H, Xu M, Zang J, Zhang Z, Ban Y, Guo S, Guo Y, Li W, Mao Y, Qian SJ, Teng H, Zhu B, Zou W, Cabrera A, Moreno BG, Rios AAO, Oliveros AFO, Sanabria JC, Godinovic N, Lelas D, Lelas K, Plestina R, Polic D, Puljak I, Antunovic Z, Dzelalija M, Brigljevic V, Duric S, Kadija K, Morovic S, Attikis A, Galanti M, Mousa J, Nicolaou C, Ptochos F, Razis PA, Finger M, Finger M, Assran Y, Kamel AE, Khalil S, Mahmoud MA, Hektor A, Kadastik M, Muntel M, Raidal M, Rebane L, Tiko A, Azzolini V, Eerola P, Fedi G, Czellar S, Harkonen J, Heikkinen A, Karimaki V, Kinnunen R, Kortelainen MJ, Lampen T, Lassila-Perini K, Lehti S, Linden T, Luukka P, Maenpaa T, Tuominen E, Tuominiemi J, Tuovinen E, Ungaro D, Wendland L, Banzuzi K, Karjalainen A, Korpela A, Tuuva T, Sillou D, Besancon M, Choudhury S, Dejardin M, Denegri D, Fabbro B, Faure JL, Ferri F, Ganjour S, Gentit FX, Givernaud A, Gras P, de Monchenault GH, Jarry P, Locci E, Malcles J, Marionneau M, Millischer L, Rander J, Rosowsky A, Shreyber I, Titov M, Verrecchia P, Baffioni S, Beaudette F, Benhabib L, Bianchini L, Bluj M, Broutin C, Busson P, Charlot C, Dahms T, Dobrzynski L, Elgammal 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Marangelli B, My S, Nuzzo S, Pacifico N, Pierro GA, Pompili A, Pugliese G, Romano F, Roselli G, Selvaggi G, Silvestris L, Trentadue R, Tupputi S, Zito G, Abbiendi G, Benvenuti AC, Bonacorsi D, Braibant-Giacomelli S, Brigliadori L, Capiluppi P, Castro A, Cavallo FR, Cuffiani M, Dallavalle GM, Fabbri F, Fanfani A, Fasanella D, Giacomelli P, Giunta M, Grandi C, Marcellini S, Masetti G, Meneghelli M, Montanari A, Navarria FL, Odorici F, Perrotta A, Primavera F, Rossi AM, Rovelli T, Siroli G, Travaglini R, Albergo S, Cappello G, Chiorboli M, Costa S, Tricomi A, Tuve C, Barbagli G, Ciulli V, Civinini C, D'Alessandro R, Focardi E, Frosali S, Gallo E, Gonzi S, Lenzi P, Meschini M, Paoletti S, Sguazzoni G, Tropiano A, Benussi L, Bianco S, Colafranceschi S, Fabbri F, Piccolo D, Fabbricatore P, Musenich R, Benaglia A, De Guio F, Di Matteo L, Gennai S, Ghezzi A, Malvezzi S, Martelli A, Massironi A, Menasce D, Moroni L, Paganoni M, Pedrini D, Ragazzi S, Redaelli N, Sala S, de Fatis TT, Buontempo S, Montoya CAC, Cavallo N, De Cosa A, Fabozzi F, Iorio AOM, Lista L, Merola M, Paolucci P, Azzi P, Bacchetta N, Bellan P, Bisello D, Branca A, Carlin R, Checchia P, Dorigo T, Dosselli U, Fanzago F, Gasparini F, Gasparini U, Gozzelino A, Lacaprara S, Lazzizzera I, Margoni M, Mazzucato M, Meneguzzo AT, Nespolo M, Perrozzi L, Pozzobon N, Ronchese P, Simonetto F, Torassa E, Tosi M, Vanini S, Zotto P, Zumerle G, Baesso P, Berzano U, Ratti SP, Riccardi C, Torre P, Vitulo P, Viviani C, Biasini M, Bilei GM, Caponeri B, Fano L, Lariccia P, Lucaroni A, Mantovani G, Menichelli M, Nappi A, Romeo F, Santocchia A, Taroni S, Valdata M, Azzurri P, Bagliesi G, Bernardini J, Boccali T, Broccolo G, Castaldi R, D'Agnolo RT, Dell'Orso R, Fiori F, Foa L, Giassi A, Kraan A, Ligabue F, Lomtadze T, Martini L, Messineo A, Palla F, Segneri G, Serban AT, Spagnolo P, Tenchini R, Tonelli G, Venturi A, Verdini PG, Barone L, Cavallari F, Del Re D, Di Marco E, Diemoz M, Franci D, Grassi M, Longo E, Meridiani P, 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Hall-Wilton R, Herndon M, Herve A, Klabbers P, Klukas J, Lanaro A, Lazaridis C, Leonard J, Loveless R, Mohapatra A, Palmonari F, Reeder D, Ross I, Savin A, Smith WH, Swanson J, Weinberg M
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Indications of Suppression of Excited Upsilon States in Pb-Pb Collisions at root(NN)-N-s=2.76 TeV
PHYSICAL REVIEW LETTERS 2011 JUL 28; 107(5):? Article 052302
A comparison of the relative yields of Upsilon resonances in the mu(+)mu(-) decay channel in Pb-Pb and pp collisions at a center-of-mass energy per nucleon pair of 2.76 TeV is performed with data collected with the CMS detector at the LHC. Using muons of transverse momentum above 4 GeV/c and pseudorapidity below 2.4, the double ratio of the Upsilon(2S) and Upsilon(3S) excited states to the Upsilon(1S) ground state in Pb-Pb and pp collisions, [Upsilon(2S + 3S)/Upsilon(1S)](Pb-Pb) /[Upsilon 2S + 3S)/Upsilon(1S)](pp), is found to be 0.31(-0.15)(+0.19) (stat_ +/- 0.03(syst). The probability to obtain the measured value, or lower, if the true double ratio is unity, is calculated to be less than 1%.
Barson JR, Morganstern I, Leibowitz SF
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Similarities in hypothalamic and mesocorticolimbic circuits regulating the overconsumption of food and alcohol
PHYSIOLOGY & BEHAVIOR 2011 JUL 25; 104(1):128-137
Historically, studies of food intake regulation started with the hypothalamus and gradually expanded to mesocorticolimbic regions, while studies of drug use began with mesocorticolimbic regions and now include the hypothalamus. As research on ingestive behavior has progressed, it has uncovered more and more similarities between the regulation of palatable food and drug intake. It has also identified specific neurochemicals involved in palatable food and drug intake. Hypothalamic orexigenic neurochemicals specifically involved in controlling fat ingestion, including galanin, enkephalin, orexin and melanin-concentrating hormone, show positive feedback with this macronutrient, with these peptides both increasing fat intake and being further stimulated by its intake. This positive relationship offers some explanation for why foods high in fat are so often overconsumed. Research in Bart Hoebel's laboratory in conjunction with our own has shown that consumption of ethanol, a drug of abuse that also contains calories, is similarly driven by these neurochemical systems involved in fat intake, consistent with evidence closely relating fat and ethanol consumption. Both fat and ethanol intake are also regulated by dopamine and acetylcholine acting in mesocorticolimbic nuclei. This close relationship of fat and ethanol is likely driven in part by circulating lipids, which are increased by fat and ethanol intake, known to increase expression and levels of the neurochemicals, and found to promote further intake of fat and ethanol. Compellingly, recent studies suggest that these systems may already be dysregulated in animals prone to consuming excess fat or ethanol, even before they have ever been exposed to these substances. Further understanding of these systems involved in consummatory behavior will allow researchers to develop effective therapies for the treatment of overeating as well as drug abuse. Published by Elsevier Inc.
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Measurement of the t(t)over-bar production cross section and the top quark mass in the dilepton channel in pp collisions at root s=7 Tev
JOURNAL OF HIGH ENERGY PHYSICS 2011 JUL; ?(7):? Article 049
The t (t) over bar production cross section and top quark mass are measured in proton-proton collisions at root s = 7 TeV in a data sample corresponding to an integrated luminosity of 36 pb(-1) collected by the CMS experiment. The measurements are performed in events with two leptons (electrons or muons) in the final state. Results of the cross section measurement in events with and without b-quark identification are obtained and combined. The measured value is sigma(tt) - 168 +/- 18 (stat:) +/- 14 (syst:) +/- 7 (lumi:) pb, consistent with predictions from the standard model. The top quark mass m(top) is reconstructed with two different methods, a full kinematic analysis and a matrix weighting technique. The combination yields a measurement of m(top) = 175.5 +/- 4.6 (stat:) +/- 4: 6 (syst:) GeV/c(2).
Engmann O, Hortobagyi T, Thompson AJ, Guadagno J, Troakes C, Soriano S, Al-Sarraj S, Kim Y, Giese KP
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Cyclin-Dependent Kinase 5 Activator p25 Is Generated During Memory Formation and Is Reduced at an Early Stage in Alzheimer's Disease
BIOLOGICAL PSYCHIATRY 2011 JUL 15; 70(2):159-168
Background: The cyclin-dependent kinase 5 activator p35 can be cleaved into p25. Formation of p25 has been suggested to contribute to neurodegeneration in Alzheimer's disease (AD). However, overexpression of low levels of p25 in mice enhances memory formation. Therefore, it has been suggested that p25 formation might be an event early in AD to compensate for impairments in synaptic plasticity. Ongoing p25 formation has been hypothesized to contribute to neurodegeneration at the later stages of AD. Methods: Here, we tested the early compensation hypothesis by analyzing the levels of p25 and its precursor p35 in AD postmortem samples from different brain regions at different stages of tau pathology, using quantitative Western blots. Furthermore, we studied p35 and p25 during spatial memory formation. By employing quantitative mass spectrometry, we identified proteins downstream of p25, which were then studied in AD samples. Results: We found that p25 is generated during spatial memory formation. Furthermore, we demonstrate that overexpression of p25 in the physiological range increases the expression of two proteins implicated in spine formation, septin 7 and optic atrophy 1. We show that the expression of p35 and p25 is reduced as an early event in AD. Moreover, expression of the p25-regulated protein optic atrophy 1 was reduced in a time course similar to p25 expression. Conclusions: Our findings suggest that p25 generation is a mechanism underlying hippocampal memory formation that is impaired in the early stages of AD. Our findings argue against the previously raised early compensation hypothesis and they propose that p25-mediated neurotoxicity does not occur in AD.
Aaltonen T, Gonzalez BA, Amerio S, Amidei D, Anastassov A, Annovi A, Antos J, Apollinari G, Appel JA, Apresyan A, Arisawa T, Artikov A, Asaadi J, Ashmanskas W, Auerbach B, Aurisano A, Azfar F, Badgett W, Barbaro-Galtieri A, Barnes VE, Barnett BA, Barria P, Bartos P, Bauce M, Bauer G, Bedeschi F, Beecher D, Behari S, Bellettini G, Bellinger J, Benjamin D, Beretvas A, Bhatti A, Binkley M, Bisello D, Bizjak I, Bland KR, Blumenfeld B, Bocci A, Bodek A, Bortoletto D, Boudreau J, Boveia A, Brau B, Brigliadori L, Brisuda A, Bromberg C, Brucken E, Bucciantonio M, Budagov J, Budd HS, Budd S, Burkett K, Busetto G, Bussey P, Buzatu A, Calancha C, Camarda S, Campanelli M, Campbell M, Canelli F, Canepa A, Carls B, Carlsmith D, Carosi R, Carrillo S, Carron S, Casal B, Casarsa M, Castro A, Catastini P, Cauz D, Cavaliere V, Cavalli-Sforza M, Cerri A, Cerrito L, Chen YC, Chertok M, Chiarelli G, Chlachidze G, Chlebana F, Cho K, Chokheli D, Chou JP, Chung WH, Chung YS, Ciobanu CI, Ciocci MA, Clark A, Compostella G, Convery ME, Conway J, Corbo M, Cordelli M, Cox CA, Cox DJ, Crescioli F, Almenar CC, Cuevas J, Culbertson R, Dagenhart D, d'Ascenzo N, Datta M, de Barbaro P, De Cecco S, De Lorenzo G, Dell'Orso M, Deluca C, Demortier L, Deng J, Deninno M, Devoto F, d'Errico M, Di Canto A, Di Ruzza B, Dittmann JR, D'Onofrio M, Donati S, Dong P, Dorigo M, Dorigo T, Ebina K, Elagin A, Eppig A, Erbacher R, Errede D, Errede S, Ershaidat N, Eusebi R, Fang HC, Farrington S, Feindt M, Fernandez JP, Ferrazza C, Field R, Flanagan G, Forrest R, Frank MJ, Franklin M, Freeman JC, Funakoshi Y, Furic I, Gallinaro M, Galyardt J, Garcia JE, Garfinkel AF, Garosi P, Gerberich H, Gerchtein E, Giagu S, Giakoumopoulou V, Giannetti P, Gibson K, Ginsburg CM, Giokaris N, Giromini P, Giunta M, Giurgiu G, Glagolev V, Glenzinski D, Gold M, Goldin D, Goldschmidt N, Golossanov A, Gomez G, Gomez-Ceballos G, Goncharov M, Gonzalez O, Gorelov I, Goshaw AT, Goulianos K, Grinstein S, Grosso-Pilcher C, Group RC, da Costa JG, Gunay-Unalan Z, Haber C, Hahn SR, Halkiadakis E, Hamaguchi A, Han JY, Happacher F, Hara K, Hare D, Hare M, Harr RF, Hatakeyama K, Hays C, Heck M, Heinrich J, Herndon M, Hewamanage S, Hidas D, Hocker A, Hopkins W, Horn D, Hou S, Hughes RE, Hurwitz M, Husemann U, Hussain N, Hussein M, Huston J, Introzzi G, Iori M, Ivanov A, James E, Jang D, Jayatilaka B, Jeon EJ, Jha MK, Jindariani S, Johnson W, Jones M, Joo KK, Jun SY, Junk TR, Kamon T, Karchin PE, Kasmi A, Kato Y, Ketchum W, Keung J, Khotilovich V, Kilminster B, Kim DH, Kim HS, Kim HW, Kim JE, Kim MJ, Kim SB, Kim SH, Kim YK, Kimura N, Kirby M, Klimenko S, Kondo K, Kong DJ, Konigsberg J, Kotwal AV, Kreps M, Kroll J, Krop D, Krumnack N, Kruse M, Krutelyov V, Kuhr T, Kurata M, Kwang S, Laasanen AT, Lami S, Lammel S, Lancaster M, Lander RL, Lannon K, Lath A, Latino G, LeCompte T, Lee E, Lee HS, Lee JS, Lee SW, Leo S, Leone S, Lewis JD, Limosani A, Lin CJ, Linacre J, Lindgren M, Lipeles E, Lister A, Litvintsev DO, Liu C, Liu Q, Liu T, Lockwitz S, Lockyer NS, Loginov A, Lucchesi D, Lueck J, Lujan P, Lukens P, Lungu G, Lys J, Lysak R, Madrak R, Maeshima K, Makhoul K, Maksimovic P, Malik S, Manca G, Manousakis-Katsikakis A, Margaroli F, Marino C, Martinez M, Martinez-Ballarin R, Mastrandrea P, Mathis M, Mattson ME, Mazzanti P, McFarland KS, McIntyre P, McNulty R, Mehta A, Mehtala P, Menzione A, Mesropian C, Miao T, Mietlicki D, Mitra A, Miyake H, Moed S, Moggi N, Mondragon MN, Moon CS, Moore R, Morello MJ, Morlock J, Fernandez PM, Mukherjee A, Muller T, Murat P, Mussini M, Nachtman J, Nagai Y, Naganoma J, Nakano I, Napier A, Nett J, Neu C, Neubauer MS, Nielsen J, Nodulman L, Norniella O, Nurse E, Oakes L, Oh SH, Oh YD, Oksuzian I, Okusawa T, Orava R, Ortolan L, Griso SP, Pagliarone C, Palencia E, Papadimitriou V, Paramonov AA, Patrick J, Pauletta G, Paulini M, Paus C, Pellett DE, Penzo A, Phillips TJ, Piacentino G, Pianori E, Pilot J, Pitts K, Plager C, Pondrom L, Potamianos K, Poukhov O, Prokoshin F, Pronko A, Ptohos F, Pueschel E, Punzi G, Pursley J, Rahaman A, Ramakrishnan V, Ranjan N, Redondo I, Renton P, Rescigno M, Rimondi F, Ristori L, Robson A, Rodrigo T, Rodriguez T, Rogers E, Rolli S, Roser R, Rossi M, Rubbo F, Ruffini F, Ruiz A, Russ J, Rusu V, Safonov A, Sakumoto WK, Sakurai Y, Santi L, Sartori L, Sato K, Saveliev V, Savoy-Navarro A, Schlabach P, Schmidt A, Schmidt EE, Schmidt MP, Schmitt M, Schwarz T, Scodellaro L, Scribano A, Scuri F, Sedov A, Seidel S, Seiya Y, Semenov A, Sforza F, Sfyrla A, Shalhout SZ, Shears T, Shepard PF, Shimojima M, Shiraishi S, Shochet M, Shreyber I, Simonenko A, Sinervo P, Sissakian A, Sliwa K, Smith JR, Snider FD, Soha A, Somalwar S, Sorin V, Squillacioti P, Stancari M, Stanitzki M, St Denis R, Stelzer B, Stelzer-Chilton O, Stentz D, Strologas J, Strycker GL, Sudo Y, Sukhanov A, Suslov I, Takemasa K, Takeuchi Y, Tang J, Tecchio M, Teng PK, Thom J, Thome J, Thompson GA, Thomson E, Ttito-Guzman P, Tkaczyk S, Toback D, Tokar S, Tollefson K, Tomura T, Tonelli D, Torre S, Torretta D, Totaro P, Trovato M, Tu Y, Ukegawa F, Uozumi S, Varganov A, Vazquez F, Velev G, Vellidis C, Vidal M, Vila I, Vilar R, Vizan J, Vogel M, Volpi G, Wagner P, Wagner RL, Wakisaka T, Wallny R, Wang SM, Warburton A, Waters D, Weinberger M, Wester WC, Whitehouse B, Whiteson D, Wicklund AB, Wicklund E, Wilbur S, Wick F, Williams HH, Wilson JS, Wilson P, Winer BL, Wittich P, Wolbers S, Wolfe H, Wright T, Wu X, Wu Z, Yamamoto K, Yamaoka J, Yang T, Yang UK, Yang YC, Yao WM, Yeh GP, Yi K, Yoh J, Yorita K, Yoshida T, Yu GB, Yu I, Yu SS, Yun JC, Zanetti A, Zeng Y, Zucchelli S
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Search for New Dielectron Resonances and Randall-Sundrum Gravitons at the Collider Detector at Fermilab
PHYSICAL REVIEW LETTERS 2011 JUL 27; 107(5):? Article 051801
A search for new dielectron-mass resonances using data recorded by the CDF II detector and corresponding to an integrated luminosity of 5.7 fb(-1) is presented. No significant excess over the expected standard model prediction is observed. In this data set, an event with the highest dielectron mass ever observed (960 GeV/c(2)) was recorded. The results are interpreted in the Randall-Sundrum (RS) model. Combined with the 5: 4 fb(-1) diphoton analysis, the RS-graviton lower-mass limit for the coupling k/(M) over bar (P1) = 0.1 is 1058 GeV/c(2), making it the strongest limit to date.
Zhang ZQ, Hou DF, Ren HC, Yin L
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The subleading term of the strong coupling expansion of the heavy-quark potential in a N=4 super Yang-Mills plasma
JOURNAL OF HIGH ENERGY PHYSICS 2011 JUL; ?(7):? Article 035
Applying the AdS/CFT correspondence, the expansion of the heavy-quark potential of the N = 4 supersymmetric Yang-Mills theory at large N(c) is carried out to the sub-leading term in the large 't Hooft coupling at a nonzero temperature. The strong coupling corresponds to the semi-classical expansion of the string-sigma model, the gravity dual of the Wilson loop operator, with the sub-leading term expressed in terms of functional determinants of fluctuations. The contribution of these determinants are evaluated numerically.
Rousselet E, Marcinkiewicz J, Kriz J, Zhou A, Hatten ME, Prat A, Seidah NG
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PCSK9 reduces the protein levels of the LDL receptor in mouse brain during development and after ischemic stroke
JOURNAL OF LIPID RESEARCH 2011 JUL; 52(7):1383-1391
Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a major role in cholesterol homeostasis through enhanced degradation of the LDL receptor (LDLR) in liver. As novel inhibitors/silencers of PCSK9 are now being tested in clinical trials to treat hypercholesterolemia, it is crucial to define the physiological consequences of the lack of PCSK9 in various organs. LDLR regulation by PCSK9 has not been extensively described during mouse brain development and injury. Herein, we show that PCSK9 and LDLR are co-expressed in mouse brain during development and at adulthood. Although the protein levels of LDLR and apolipoprotein E (apoE) in the adult brain of Pcsk9(-/-) mice are similar to those of wild-type (WT) mice, LDLR levels increased and were accompanied by a reduction of apoE levels during development. This suggests that the upregulation of LDLR protein levels in Pcsk9(-/-) mice enhances apoE degradation. Upon ischemic stroke, PCSK9 was expressed in the dentate gyrus between 24 h and 72 h following brain reperfusion. Although mouse behavior and lesion volume were similar, LDLR protein levels dropped similar to 2-fold less in the Pcsk9(-/-) -lesioned hippocampus, without affecting apoE levels and neurogenesis. Thus, PCSK9 downregulates LDLR levels during brain development and following transient ischemic stroke in adult mice.-Rousselet, E., J. Marcinkiewicz, J. Kriz, A. Zhou, M. E. Hatten, A. Prat, and N. G. Seidah. PCSK9 reduces the protein levels of the LDL receptor in mouse brain during development and after ischemic stroke. J. Lipid Res. 2011. 52: 1383-1391.
Teplova M, Malinina L, Darnell JC, Song JK, Lu M, Abagyan R, Musunuru K, Teplov A, Burley SK, Darnell RB, Patel DJ
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Protein-RNA and Protein-Protein Recognition by Dual KH1/2 Domains of the Neuronal Splicing Factor Nova-1
STRUCTURE 2011 JUL 13; 19(7):930-944
Nova onconeural antigens are neuron-specific RNA-binding proteins implicated in paraneoplastic opsoclonus-myoclonus-ataxia (POMA) syndrome. Nova harbors three K-homology (KH) motifs implicated in alternate splicing regulation of genes involved in inhibitory synaptic transmission. We report the crystal structure of the first two KH domains (KH1/2) of Nova-1 bound to an in vitro selected RNA hairpin, containing a UCAG-UCAC high-affinity binding site. Sequence-specific intermolecular contacts in the complex involve KH1 and the second UCAC repeat, with the RNA scaffold buttressed by interactions between repeats. Whereas the canonical RNA-binding surface of KH2 in the above complex engages in protein-protein interactions in the crystalline state, the individual KH2 domain can sequence-specifically target the UCAC RNA element in solution. The observed antiparallel alignment of KH1 and KH2 domains in the crystal structure of the complex generates a scaffold that could facilitate target pre-mRNA looping on Nova binding, thereby potentially explaining Nova's functional role in splicing regulation.