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Evan Eichler

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https://www.readbyqxmd.com/read/29776991/inversion-variants-in-human-and-primate-genomes
#1
Claudia Rita Catacchio, Flavia Angela Maria Maggiolini, Pietro D'Addabbo, Miriana Bitonto, Oronzo Capozzi, Martina Lepore Signorile, Mattia Miroballo, Nicoletta Archidiacono, Evan E Eichler, Mario Ventura, Francesca Antonacci
For many years, inversions have been proposed to be a direct driving force in speciation since they suppress recombination when heterozygous. Inversions are the most common large-scale differences among humans and great apes. Nevertheless, they represent large events easily distinguishable by classical cytogenetics, whose resolution, however, is limited. Here, we performed a genome-wide comparison between human, great ape, and macaque genomes using the net alignments for the most recent releases of genome assemblies...
May 18, 2018: Genome Research
https://www.readbyqxmd.com/read/29724491/clinical-presentation-of-a-complex-neurodevelopmental-disorder-caused-by-mutations-in-adnp
#2
Anke Van Dijck, Anneke T Vulto-van Silfhout, Elisa Cappuyns, Ilse M van der Werf, Grazia M Mancini, Andreas Tzschach, Raphael Bernier, Illana Gozes, Evan E Eichler, Corrado Romano, Anna Lindstrand, Ann Nordgren, Malin Kvarnung, Tjitske Kleefstra, Bert B A de Vries, Sébastien Küry, Jill A Rosenfeld, Marije E Meuwissen, Geert Vandeweyer, R Frank Kooy
BACKGROUND: In genome-wide screening studies for de novo mutations underlying autism and intellectual disability, mutations in the ADNP gene are consistently reported among the most frequent. ADNP mutations have been identified in children with autism spectrum disorder comorbid with intellectual disability, distinctive facial features, and deficits in multiple organ systems. However, a comprehensive clinical description of the Helsmoortel-Van der Aa syndrome is lacking. METHODS: We identified a worldwide cohort of 78 individuals with likely disruptive mutations in ADNP from January 2014 to October 2016 through systematic literature search, by contacting collaborators, and through direct interaction with parents...
March 15, 2018: Biological Psychiatry
https://www.readbyqxmd.com/read/29686068/recurrent-structural-variation-clustered-sites-of-selection-and-disease-risk-for-the-complement-factor-h-cfh-gene-family
#3
Stuart Cantsilieris, Bradley J Nelson, John Huddleston, Carl Baker, Lana Harshman, Kelsi Penewit, Katherine M Munson, Melanie Sorensen, AnneMarie E Welch, Vy Dang, Felix Grassmann, Andrea J Richardson, Robyn H Guymer, Tina A Graves-Lindsay, Richard K Wilson, Bernhard H F Weber, Paul N Baird, Rando Allikmets, Evan E Eichler
Structural variation and single-nucleotide variation of the complement factor H ( CFH ) gene family underlie several complex genetic diseases, including age-related macular degeneration (AMD) and atypical hemolytic uremic syndrome (AHUS). To understand its diversity and evolution, we performed high-quality sequencing of this ∼360-kbp locus in six primate lineages, including multiple human haplotypes. Comparative sequence analyses reveal two distinct periods of gene duplication leading to the emergence of four CFH -related ( CFHR ) gene paralogs ( CFHR2 and CFHR4 ∼25-35 Mya and CFHR1 and CFHR3 ∼7-13 Mya)...
April 23, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29674745/publisher-correction-the-sea-lamprey-germline-genome-provides-insights-into-programmed-genome-rearrangement-and-vertebrate-evolution
#4
Jeramiah J Smith, Nataliya Timoshevskaya, Chengxi Ye, Carson Holt, Melissa C Keinath, Hugo J Parker, Malcolm E Cook, Jon E Hess, Shawn R Narum, Francesco Lamanna, Henrik Kaessmann, Vladimir A Timoshevskiy, Courtney K M Waterbury, Cody Saraceno, Leanne M Wiedemann, Sofia M C Robb, Carl Baker, Evan E Eichler, Dorit Hockman, Tatjana Sauka-Spengler, Mark Yandell, Robb Krumlauf, Greg Elgar, Chris T Amemiya
In the version of this article initially published, the present addresses for authors Dorit Hockman and Chris Amemiya were switched. The error has been corrected in the HTML and PDF versions of the article.
April 19, 2018: Nature Genetics
https://www.readbyqxmd.com/read/29656860/truncating-variants-in-naa15-are-associated-with-variable-levels-of-intellectual-disability-autism-spectrum-disorder-and-congenital-anomalies
#5
Hanyin Cheng, Avinash V Dharmadhikari, Sylvia Varland, Ning Ma, Deepti Domingo, Robert Kleyner, Alan F Rope, Margaret Yoon, Asbjørg Stray-Pedersen, Jennifer E Posey, Sarah R Crews, Mohammad K Eldomery, Zeynep Coban Akdemir, Andrea M Lewis, Vernon R Sutton, Jill A Rosenfeld, Erin Conboy, Katherine Agre, Fan Xia, Magdalena Walkiewicz, Mauro Longoni, Frances A High, Marjon A van Slegtenhorst, Grazia M S Mancini, Candice R Finnila, Arie van Haeringen, Nicolette den Hollander, Claudia Ruivenkamp, Sakkubai Naidu, Sonal Mahida, Elizabeth E Palmer, Lucinda Murray, Derek Lim, Parul Jayakar, Michael J Parker, Stefania Giusto, Emanuela Stracuzzi, Corrado Romano, Jennifer S Beighley, Raphael A Bernier, Sébastien Küry, Mathilde Nizon, Mark A Corbett, Marie Shaw, Alison Gardner, Christopher Barnett, Ruth Armstrong, Karin S Kassahn, Anke Van Dijck, Geert Vandeweyer, Tjitske Kleefstra, Jolanda Schieving, Marjolijn J Jongmans, Bert B A de Vries, Rolph Pfundt, Bronwyn Kerr, Samantha K Rojas, Kym M Boycott, Richard Person, Rebecca Willaert, Evan E Eichler, R Frank Kooy, Yaping Yang, Joseph C Wu, James R Lupski, Thomas Arnesen, Gregory M Cooper, Wendy K Chung, Jozef Gecz, Holly A F Stessman, Linyan Meng, Gholson J Lyon
N-alpha-acetylation is a common co-translational protein modification that is essential for normal cell function in humans. We previously identified the genetic basis of an X-linked infantile lethal Mendelian disorder involving a c.109T>C (p.Ser37Pro) missense variant in NAA10, which encodes the catalytic subunit of the N-terminal acetyltransferase A (NatA) complex. The auxiliary subunit of the NatA complex, NAA15, is the dimeric binding partner for NAA10. Through a genotype-first approach with whole-exome or genome sequencing (WES/WGS) and targeted sequencing analysis, we identified and phenotypically characterized 38 individuals from 33 unrelated families with 25 different de novo or inherited, dominantly acting likely gene disrupting (LGD) variants in NAA15...
April 9, 2018: American Journal of Human Genetics
https://www.readbyqxmd.com/read/29474918/dissecting-the-causal-mechanism-of-x-linked-dystonia-parkinsonism-by-integrating-genome-and-transcriptome-assembly
#6
Tatsiana Aneichyk, William T Hendriks, Rachita Yadav, David Shin, Dadi Gao, Christine A Vaine, Ryan L Collins, Aloysius Domingo, Benjamin Currall, Alexei Stortchevoi, Trisha Multhaupt-Buell, Ellen B Penney, Lilian Cruz, Jyotsna Dhakal, Harrison Brand, Carrie Hanscom, Caroline Antolik, Marisela Dy, Ashok Ragavendran, Jason Underwood, Stuart Cantsilieris, Katherine M Munson, Evan E Eichler, Patrick Acuña, Criscely Go, R Dominic G Jamora, Raymond L Rosales, Deanna M Church, Stephen R Williams, Sarah Garcia, Christine Klein, Ulrich Müller, Kirk C Wilhelmsen, H T Marc Timmers, Yechiam Sapir, Brian J Wainger, Daniel Henderson, Naoto Ito, Neil Weisenfeld, David Jaffe, Nutan Sharma, Xandra O Breakefield, Laurie J Ozelius, D Cristopher Bragg, Michael E Talkowski
X-linked Dystonia-Parkinsonism (XDP) is a Mendelian neurodegenerative disease that is endemic to the Philippines and is associated with a founder haplotype. We integrated multiple genome and transcriptome assembly technologies to narrow the causal mutation to the TAF1 locus, which included a SINE-VNTR-Alu (SVA) retrotransposition into intron 32 of the gene. Transcriptome analyses identified decreased expression of the canonical cTAF1 transcript among XDP probands, and de novo assembly across multiple pluripotent stem-cell-derived neuronal lineages discovered aberrant TAF1 transcription that involved alternative splicing and intron retention (IR) in proximity to the SVA that was anti-correlated with overall TAF1 expression...
February 22, 2018: Cell
https://www.readbyqxmd.com/read/29375855/longitudinal-report-of-child-with-de-novo-16p11-2-triplication
#7
Arianne S Wallace, Caitlin M Hudac, Kyle J Steinman, Jessica L Peterson, Trent D DesChamps, Michael H Duyzend, Xander Nuttle, Evan E Eichler, Raphael A Bernier
16p11.2 deletions and duplications are commonly associated with autism spectrum disorder and linked to mirrored phenotypes of physical characteristics and higher penetrance for deletions. A male with a rare 16p11.2 triplication demonstrated a similar phenotypic presentation to deletion carriers with neurocognitive and adaptive skill deficits and above-average physical growth.
January 2018: Clinical Case Reports
https://www.readbyqxmd.com/read/29358652/the-sea-lamprey-germline-genome-provides-insights-into-programmed-genome-rearrangement-and-vertebrate-evolution
#8
Jeramiah J Smith, Nataliya Timoshevskaya, Chengxi Ye, Carson Holt, Melissa C Keinath, Hugo J Parker, Malcolm E Cook, Jon E Hess, Shawn R Narum, Francesco Lamanna, Henrik Kaessmann, Vladimir A Timoshevskiy, Courtney K M Waterbury, Cody Saraceno, Leanne M Wiedemann, Sofia M C Robb, Carl Baker, Evan E Eichler, Dorit Hockman, Tatjana Sauka-Spengler, Mark Yandell, Robb Krumlauf, Greg Elgar, Chris T Amemiya
The sea lamprey (Petromyzon marinus) serves as a comparative model for reconstructing vertebrate evolution. To enable more informed analyses, we developed a new assembly of the lamprey germline genome that integrates several complementary data sets. Analysis of this highly contiguous (chromosome-scale) assembly shows that both chromosomal and whole-genome duplications have played significant roles in the evolution of ancestral vertebrate and lamprey genomes, including chromosomes that carry the six lamprey HOX clusters...
February 2018: Nature Genetics
https://www.readbyqxmd.com/read/29295848/corrigendum-discovery-and-genotyping-of-structural-variation-from-long-read-haploid-genome-sequence-data
#9
John Huddleston, Mark J P Chaisson, Karyn Meltz Steinberg, Wes Warren, Kendra Hoekzema, David Gordon, Tina A Graves-Lindsay, Katherine M Munson, Zev N Kronenberg, Laura Vives, Paul Peluso, Matthew Boitano, Chen-Shin Chin, Jonas Korlach, Richard K Wilson, Evan E Eichler
No abstract text is available yet for this article.
January 2018: Genome Research
https://www.readbyqxmd.com/read/29250444/associations-between-familial-rates-of-psychiatric-disorders-and-de-novo-genetic-mutations-in-autism
#10
Kyleen Luhrs, Tracey Ward, Caitlin M Hudac, Jennifer Gerdts, Holly A F Stessman, Evan E Eichler, Raphael A Bernier
The purpose of this study was to examine the confluence of genetic and familial risk factors in children with Autism Spectrum Disorder (ASD) with distinct de novo genetic events. We hypothesized that gene-disrupting mutations would be associated with reduced rates of familial psychiatric disorders relative to structural mutations. Participants included families of children with ASD in four groups: de novo duplication copy number variations (DUP, n = 62), de novo deletion copy number variations (DEL, n = 74), de novo likely gene-disrupting mutations (LGDM, n = 267), and children without a known genetic etiology (NON, n = 2111)...
2017: Autism Research and Treatment
https://www.readbyqxmd.com/read/29209020/a-genotype-first-approach-identifies-an-intellectual-disability-overweight-syndrome-caused-by-phip-haploinsufficiency
#11
Sandra Jansen, Alexander Hoischen, Bradley P Coe, Gemma L Carvill, Hilde Van Esch, Daniëlle G M Bosch, Ulla A Andersen, Carl Baker, Marijke Bauters, Raphael A Bernier, Bregje W van Bon, Hedi L Claahsen-van der Grinten, Jozef Gecz, Christian Gilissen, Lucia Grillo, Anna Hackett, Tjitske Kleefstra, David Koolen, Malin Kvarnung, Martin J Larsen, Carlo Marcelis, Fiona McKenzie, Marie-Lorraine Monin, Caroline Nava, Janneke H Schuurs-Hoeijmakers, Rolph Pfundt, Marloes Steehouwer, Servi J C Stevens, Connie T Stumpel, Fleur Vansenne, Mirella Vinci, Maartje van de Vorst, Petra de Vries, Kali Witherspoon, Joris A Veltman, Han G Brunner, Heather C Mefford, Corrado Romano, Lisenka E L M Vissers, Evan E Eichler, Bert B A de Vries
Genotype-first combined with reverse phenotyping has shown to be a powerful tool in human genetics, especially in the era of next generation sequencing. This combines the identification of individuals with mutations in the same gene and linking these to consistent (endo)phenotypes to establish disease causality. We have performed a MIP (molecular inversion probe)-based targeted re-sequencing study in 3,275 individuals with intellectual disability (ID) to facilitate a genotype-first approach for 24 genes previously implicated in ID...
January 2018: European Journal of Human Genetics: EJHG
https://www.readbyqxmd.com/read/29179772/recurrent-de-novo-mutations-in-neurodevelopmental-disorders-properties-and-clinical-implications
#12
REVIEW
Amy B Wilfert, Arvis Sulovari, Tychele N Turner, Bradley P Coe, Evan E Eichler
Next-generation sequencing (NGS) is now more accessible to clinicians and researchers. As a result, our understanding of the genetics of neurodevelopmental disorders (NDDs) has rapidly advanced over the past few years. NGS has led to the discovery of new NDD genes with an excess of recurrent de novo mutations (DNMs) when compared to controls. Development of large-scale databases of normal and disease variation has given rise to metrics exploring the relative tolerance of individual genes to human mutation. Genetic etiology and diagnosis rates have improved, which have led to the discovery of new pathways and tissue types relevant to NDDs...
November 27, 2017: Genome Medicine
https://www.readbyqxmd.com/read/29100089/de-novo-mutations-in-protein-kinase-genes-camk2a-and-camk2b-cause-intellectual-disability
#13
Sébastien Küry, Geeske M van Woerden, Thomas Besnard, Martina Proietti Onori, Xénia Latypova, Meghan C Towne, Megan T Cho, Trine E Prescott, Melissa A Ploeg, Stephan Sanders, Holly A F Stessman, Aurora Pujol, Ben Distel, Laurie A Robak, Jonathan A Bernstein, Anne-Sophie Denommé-Pichon, Gaëtan Lesca, Elizabeth A Sellars, Jonathan Berg, Wilfrid Carré, Øyvind Løvold Busk, Bregje W M van Bon, Jeff L Waugh, Matthew Deardorff, George E Hoganson, Katherine B Bosanko, Diana S Johnson, Tabib Dabir, Øystein Lunde Holla, Ajoy Sarkar, Kristian Tveten, Julitta de Bellescize, Geir J Braathen, Paulien A Terhal, Dorothy K Grange, Arie van Haeringen, Christina Lam, Ghayda Mirzaa, Jennifer Burton, Elizabeth J Bhoj, Jessica Douglas, Avni B Santani, Addie I Nesbitt, Katherine L Helbig, Marisa V Andrews, Amber Begtrup, Sha Tang, Koen L I van Gassen, Jane Juusola, Kimberly Foss, Gregory M Enns, Ute Moog, Katrin Hinderhofer, Nagarajan Paramasivam, Sharyn Lincoln, Brandon H Kusako, Pierre Lindenbaum, Eric Charpentier, Catherine B Nowak, Elouan Cherot, Thomas Simonet, Claudia A L Ruivenkamp, Sihoun Hahn, Catherine A Brownstein, Fan Xia, Sébastien Schmitt, Wallid Deb, Dominique Bonneau, Mathilde Nizon, Delphine Quinquis, Jamel Chelly, Gabrielle Rudolf, Damien Sanlaville, Philippe Parent, Brigitte Gilbert-Dussardier, Annick Toutain, Vernon R Sutton, Jenny Thies, Lisenka E L M Peart-Vissers, Pierre Boisseau, Marie Vincent, Andreas M Grabrucker, Christèle Dubourg, Wen-Hann Tan, Nienke E Verbeek, Martin Granzow, Gijs W E Santen, Jay Shendure, Bertrand Isidor, Laurent Pasquier, Richard Redon, Yaping Yang, Matthew W State, Tjitske Kleefstra, Benjamin Cogné, Slavé Petrovski, Kyle Retterer, Evan E Eichler, Jill A Rosenfeld, Pankaj B Agrawal, Stéphane Bézieau, Sylvie Odent, Ype Elgersma, Sandra Mercier
Calcium/calmodulin-dependent protein kinase II (CAMK2) is one of the first proteins shown to be essential for normal learning and synaptic plasticity in mice, but its requirement for human brain development has not yet been established. Through a multi-center collaborative study based on a whole-exome sequencing approach, we identified 19 exceedingly rare de novo CAMK2A or CAMK2B variants in 24 unrelated individuals with intellectual disability. Variants were assessed for their effect on CAMK2 function and on neuronal migration...
November 2, 2017: American Journal of Human Genetics
https://www.readbyqxmd.com/read/29092041/a-3-way-hybrid-approach-to-generate-a-new-high-quality-chimpanzee-reference-genome-pan_tro_3-0
#14
Lukas F K Kuderna, Chad Tomlinson, LaDeana W Hillier, Annabel Tran, Ian T Fiddes, Joel Armstrong, Hafid Laayouni, David Gordon, John Huddleston, Raquel Garcia Perez, Inna Povolotskaya, Aitor Serres Armero, Jèssica Gómez Garrido, Daniel Ho, Paolo Ribeca, Tyler Alioto, Richard E Green, Benedict Paten, Arcadi Navarro, Jaume Betranpetit, Javier Herrero, Evan E Eichler, Andrew J Sharp, Lars Feuk, Wesley C Warren, Tomas Marques-Bonet
The chimpanzee is arguably the most important species for the study of human origins. A key resource for these studies is a high-quality reference genome assembly; however, as with most mammalian genomes, the current iteration of the chimpanzee reference genome assembly is highly fragmented. In the current iteration of the chimpanzee reference genome assembly (Pan_tro_2.1.4), the sequence is scattered across more then 183 000 contigs, incorporating more than 159 000 gaps, with a genome-wide contig N50 of 51 Kbp...
November 1, 2017: GigaScience
https://www.readbyqxmd.com/read/29090079/prospective-investigation-of-foxp1-syndrome
#15
Paige M Siper, Silvia De Rubeis, Maria Del Pilar Trelles, Allison Durkin, Daniele Di Marino, François Muratet, Yitzchak Frank, Reymundo Lozano, Evan E Eichler, Morgan Kelly, Jennifer Beighley, Jennifer Gerdts, Arianne S Wallace, Heather C Mefford, Raphael A Bernier, Alexander Kolevzon, Joseph D Buxbaum
BACKGROUND: Haploinsufficiency of the forkhead-box protein P1 ( FOXP1 ) gene leads to a neurodevelopmental disorder termed FOXP1 syndrome. Previous studies in individuals carrying FOXP1 mutations and deletions have described the presence of autism spectrum disorder (ASD) traits, intellectual disability, language impairment, and psychiatric features. The goal of the present study was to comprehensively characterize the genetic and clinical spectrum of FOXP1 syndrome. This is the first study to prospectively examine the genotype-phenotype relationship in multiple individuals with FOXP1 syndrome, using a battery of standardized clinical assessments...
2017: Molecular Autism
https://www.readbyqxmd.com/read/29034068/clinical-phenotype-of-asd-associated-dyrk1a-haploinsufficiency
#16
Rachel K Earl, Tychele N Turner, Heather C Mefford, Caitlin M Hudac, Jennifer Gerdts, Evan E Eichler, Raphael A Bernier
BACKGROUND: DYRK1A is a gene recurrently disrupted in 0.1-0.5% of the ASD population. A growing number of case reports with DYRK1A haploinsufficiency exhibit common phenotypic features including microcephaly, intellectual disability, speech delay, and facial dysmorphisms. METHODS: Phenotypic information from previously published DYRK1A cases ( n  = 51) and participants in an ongoing study at the University of Washington (UW, n  = 10) were compiled. Frequencies of recurrent phenotypic features in this population were compared to features observed in a large sample with idiopathic ASD from the Simons Simplex Collection ( n  = 1981)...
2017: Molecular Autism
https://www.readbyqxmd.com/read/28982794/a-high-coverage-neandertal-genome-from-vindija-cave-in-croatia
#17
Kay Prüfer, Cesare de Filippo, Steffi Grote, Fabrizio Mafessoni, Petra Korlević, Mateja Hajdinjak, Benjamin Vernot, Laurits Skov, Pinghsun Hsieh, Stéphane Peyrégne, David Reher, Charlotte Hopfe, Sarah Nagel, Tomislav Maricic, Qiaomei Fu, Christoph Theunert, Rebekah Rogers, Pontus Skoglund, Manjusha Chintalapati, Michael Dannemann, Bradley J Nelson, Felix M Key, Pavao Rudan, Željko Kućan, Ivan Gušić, Liubov V Golovanova, Vladimir B Doronichev, Nick Patterson, David Reich, Evan E Eichler, Montgomery Slatkin, Mikkel H Schierup, Aida M Andrés, Janet Kelso, Matthias Meyer, Svante Pääbo
To date, the only Neandertal genome that has been sequenced to high quality is from an individual found in Southern Siberia. We sequenced the genome of a female Neandertal from ~50,000 years ago from Vindija Cave, Croatia, to ~30-fold genomic coverage. She carried 1.6 differences per 10,000 base pairs between the two copies of her genome, fewer than present-day humans, suggesting that Neandertal populations were of small size. Our analyses indicate that she was more closely related to the Neandertals that mixed with the ancestors of present-day humans living outside of sub-Saharan Africa than the previously sequenced Neandertal from Siberia, allowing 10 to 20% more Neandertal DNA to be identified in present-day humans, including variants involved in low-density lipoprotein cholesterol concentrations, schizophrenia, and other diseases...
November 3, 2017: Science
https://www.readbyqxmd.com/read/28965761/genomic-patterns-of-de-novo-mutation-in-simplex-autism
#18
Tychele N Turner, Bradley P Coe, Diane E Dickel, Kendra Hoekzema, Bradley J Nelson, Michael C Zody, Zev N Kronenberg, Fereydoun Hormozdiari, Archana Raja, Len A Pennacchio, Robert B Darnell, Evan E Eichler
To further our understanding of the genetic etiology of autism, we generated and analyzed genome sequence data from 516 idiopathic autism families (2,064 individuals). This resource includes >59 million single-nucleotide variants (SNVs) and 9,212 private copy number variants (CNVs), of which 133,992 and 88 are de novo mutations (DNMs), respectively. We estimate a mutation rate of ∼1.5 × 10-8 SNVs per site per generation with a significantly higher mutation rate in repetitive DNA. Comparing probands and unaffected siblings, we observe several DNM trends...
October 19, 2017: Cell
https://www.readbyqxmd.com/read/28921525/comorbid-symptoms-of-inattention-autism-and-executive-cognition-in-youth-with-putative-genetic-risk
#19
Anne B Arnett, Brianna E Cairney, Arianne S Wallace, Jennifer Gerdts, Tychele N Turner, Evan E Eichler, Raphael A Bernier
BACKGROUND: Symptoms of autism spectrum disorder (ASD) and inattention (IA) are highly comorbid and associated with deficits in executive cognition. Cognitive deficits have been posited as candidate endophenotypes of psychiatric traits, but few studies have conceptualized cognitive deficits as psychiatric comorbidities. The latter model is consistent with a latent factor reflecting broader liability to neuropsychological dysfunction, and explains heterogeneity in the cognitive profile of individuals with ASD and IA...
March 2018: Journal of Child Psychology and Psychiatry, and Allied Disciplines
https://www.readbyqxmd.com/read/28864551/corrigendum-the-evolution-of-african-great-ape-subtelomeric-heterochromatin-and-the-fusion-of-human-chromosome-2
#20
Mario Ventura, Claudia R Catacchio, Saba Sajjadian, Laura Vives, Peter H Sudmant, Tomas Marques-Bonet, Tina A Graves, Richard K Wilson, Evan E Eichler
No abstract text is available yet for this article.
September 2017: Genome Research
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