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Inhibition of G-Protein Signalling in Cardiac Dysfunction of Intellectual J Med Genet: first published as 10.1136/jmedgenet-2020-107015 on 10 November 2020. Downloaded from http://jmg.bmj.com/ on January 14, 2021 at UCL Library Services. Protected by copyright. - - - - - 1 R) 2 6 -ad- β gated Some 4 2 1 2 8 subfamily 11 i/o retinopathy protein- 2 The former is 1 while the IDDCA 5 GNB5 Zia ur Rahman, Nicolas Guex, 6 R triggers G 2 3 The ), respectively, cause severe cause respectively, ), muscarinic receptors (M muscarinic Functional genomics - 2 4 1–10 Shazia Maqbool, subunit of guanine nucleotide- of guanine subunit SYNAPS Study Group, SYNAPS Study Group, 8 5 Hamid Galehdari, β GNB5 13 2 Reza Maroofian, Marilena Christoforou, 16 2 bipolar dysfunction, Alexandre Sarre, Javeria Raza Alvi, Raza Javeria 2 6 proteins, which turn on G- The heart rate (HR) is established by the sinoatrial established (HR) is The heart rate Anwar, Najwa 8 G- epilepsy is characterised by early seizure onset (~3 rapidly evolving seizures with focal months of age) into epileptic spasms and consequent generalised multifocal discharges. is a unique combination of dual retinal signalling of dual combination a unique is defects reminiscent of features of both bradyopsia and rod ON- present on cells innervated by parasympathetic postganglionic neurons, including sinoatrial node cells. The activation of M node, the pacemaker of the cardiac muscle, and muscle, the cardiac of pacemaker node, the controlled by the autonomic nervous system. This autonomic nervous system consists of two anatomi cally and functionally distinct divisions: the sympa thetic and the parasympathetic branches, whose work together antagonistic but often functions are In the heart, the postganglionic to maintain balance. fibres of the sympathetic trunk stimulate the renoreceptors, thereby increasing HR and force of contraction. The parasympathetic modulation of the release, acetylcholine mediated by is primarily heart M activates the which Inheritance in Man): #617173) is an autosomal recessive neurodevelopmental disorder with onset in early childhood. Inactivating and hypomorphic mutations in the binding protein ( and mild forms of the disorder. associated with cognitive disability, poor or absent with cognitive disability, associated The arrhythmias. and/or severe cardiac speech moderate manifestation of the syndrome, also named language delay and ADHD/cognitive impair (LADCI) arrhythmia ment with or without cardiac syndrome (OMIM: #617182), consists of mild attention impairment, language delay, intellectual hyperactivity disorder (ADHD) and, in about deficit arrhythmia. severe cardiac the cases, half patients with IDDCA also showed retinal dysfunc IDDCA also showed retinal patients with hypotonia and gastro tion and nystagmus, epilepsy, intestinal problems. David Murphy, 10 Alireza Sedaghat, , 11 Thierry Thierry Pedrazzini, Vincenzo Vincenzo Salpietro, mice Gnb5 15 Tipu Tipu Sultan, 5 Gnb5 −/− 1,14 encoding in heart Gnb5 binding inhibitory - protein signalling Fatima Rahman, Fatima GNB5 loss resulted in Gnb5 7 Stephanie Efthymiou, mice, an effect mice, Gnb5 1 aphy and telemetric protein signalling in cardiac −/− , , but exhibited better , Gnb5 an autosomal recessive Neda Mazaheri, +/− asympathetic control of 12 ariants of ey role of Gnb5 1 Audrey Putoux, 1 Joseph G Gleeson Gnb5 9 mice. In contrast, In contrast, mice. William F Simonds, Nicolas Chatron, , 2 −/− 14 and Homozygous Nuzhat Rana, mice were smaller and had a smaller +/+ 7 Pathogenic v Pathogenic Our data demonstrate that loss of Our data demonstrate Gnb5 −/− We used echocardiogr We Gnb5 We delineated a k We out mice. Gnb5 subunit of the guanine nucleotide- 5 β cardiac function. Lower autonomic nervous system cardiac function. control modulation through diminished parasympathetic and greater sympathetic regulation resulted in a higher baseline HR in Henry Houlden, significantly higher frequencies of sinus arrhythmias. significantly higher frequencies of sinus arrhythmias. we described 13 affected individuals, Moreover, increasing the IDDCA cohort to 44 patients. Conclusions negative regulation of the inhibitory G- causes HR perturbations in exhibited profound bradycardia on treatment with exhibited profound bradycardia while sympathetic modulation of the cardiac carbachol, transcriptome Concordantly, not altered. stimulation was study pinpointed altered expression of genes involved in atria and ventricles of in cardiac muscle contractility knocked- heart than Gholamreza Shariati, mainly driven by impaired parasympathetic activity. activity. mainly driven by impaired parasympathetic the mechanism of anticipate that unravelling We signalling in the autonomic control of the heart will pave for future drug screening. the way INTRODUCTION Alexandre Reymond Jacqueline Chrast, Jacqueline Gaetan Lesca, Intellectual developmental disorder with cardiac Intellectual (Online Mendelian OMIM (IDDCA, arrhythmia ABSTRACT Background Pasquelena De Nittis Pasquelena the ORIGINAL RESEARCH Inhibition of G- dysfunction of intellectual developmental disorder with cardiac arrhythmia (IDDCA) syndrome ECG recordings to investigate consequences of loss in mouse. Results sinus conduction and showed that neurodevelopmental disorder associated with cognitive particularly severe disability and cardiac arrhythmia, bradycardia. Methods protein cause IDDCA syndrome, (HR) and maintenance of the sympathovagal heart rate balance. signalling is essential for par Faisal Zafar, Faisal Maha S Zaki . ch . use , et al , unil 1136/ 10. 107015). Epub ahead of org/ . August 2020 2020- reymond@ De Nittis P, De Nittis P, doi . dx. Additional material is To cite: cite: To A Sarre Efthymiou S, J Med Genet [please include Day print: doi:10.1136/ Month Year]. jmedgenet-2020-107015 or numbered affiliations see © Author(s) (or their © Re- employer(s)) 2020. permitted under CC BY. Published by BMJ. ► Accepted 4 September 2020 Correspondence to Correspondence Professor Alexandre Reymond, Genomics, Center for Integrative University of Lausanne, Switzerland; Lausanne 1015, Received 19 March 2020 Revised 30 jmedgenet- end of article. published online only. To view, view, To published online only. please visit the journal online (http:// F alexandre De Nittis P, et al. J Med Genet 2020;0:1–17. doi:10.1136/jmedgenet-2020-107015 Functional genomics J Med Genet: first published as 10.1136/jmedgenet-2020-107015 on 10 November 2020. Downloaded from inwardly rectifying K+ channels (GIRK) resulting in membrane Indiana, Indianapolis, USA). Libraries were sequenced on a hyperpolarisation and decrease in HR. Regulator of G- pro- NextSeq500 (Illumina) at a mean depth coverage of 73× with tein signalling (RGS) proteins negatively regulate the timing of 93.3% of the target bases above 30×. Genomic alignment this M2R- GIRK signalling. GNB5, a divergent member of the against the hg19/GRCh37 assembly and variant calling were, Gβ family, has the unique property of forming complexes with respectively, done with BWAMEM V.0.7.12 and GATK Haplo- R7- RGS proteins.11–16 In particular, the GNB5-RGS6 complex is typeCaller V.3.4 (Broad Institute, Boston, Massachusetts, USA). involved in cardiac GIRK deactivation kinetics. Rgs6- null mice Only highly confident variants were kept for analysis (total manifested heart conduction anomalies and hypersensitivity to depth >9, alternative allele depth >4, no strand bias, mosaicism parasympathomimetics.17 Zebrafish model defective for gnb5 >10%). Rare variants were considered as having a frequency gene correspondingly showed reduced heartbeat on reinforced of <1% in GnomAD v2 dataset. Whole- exome sequencing of parasympathetic stimulation, eye movement defects and altered families X and Y was performed as described in Makrythanasis et swimming behaviour1 and cardiomyocytes differentiated from al.25 Sanger sequencing in each family confirmed the segregation human induced pluripotent stem cells (iPSCs) edited to engineer of GNB5 variants with the phenotype. the GNB5- Ser81Leu missense variant associated with LADCI showed a decrease in spontaneous activity on stimulation with 7 Mouse husbandry carbachol compared with normal cells. The Gnb5 mouse line was recovered from cryopreserved sperm Whereas homozygous Gnb5- null mice recapitulated many of using in vitro fertilisation. The knockout allele was engineered in the corresponding human disease phenotypes such as learning a C57BL/6J inbred genetic background by heterozygous deletion deficiencies, hyperactivity, impaired motor coordination and 18 22 18–22 of exon 3 in the germline, as previously described. Genet- perturbed vision, a systematic cardiac evaluation has never ically modified animals were born and housed in the Animal been performed in a mammalian model. Here, we assessed Facility of the Centre for Integrative Genomics, under controlled heart electrophysiology of Gnb5 mice models. We detected an −/− temperature conditions and a 12- hour light–dark cycle with increased frequency of sinus arrhythmias in Gnb5 animals, free access to water, normal chow and nest building material. which have a smaller heart than wild- type and Gnb5+/−, but −/− Mouse genomic DNA was extracted from ear biopsies using the exhibited better cardiac function. Gnb5 mice also displayed hot shot protocol26 and used for genotyping as described.22 To enhanced parasympathetic sensitivity on stimulation with a prevent the previously documented high mortality of Gnb5−/− cholinergic agonist. Consistent with this, transcriptome profiling pups at weaning,18 heterozygous breeding couples used to of atria and ventricles
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