Exome sequencing improves genetic diagnosis of structural fetal abnormalities revealed by ultrasound

被引:136
作者
Carss, Keren J. [1 ]
Hillman, Sarah C. [2 ]
Parthiban, Vijaya [1 ]
McMullan, Dominic J. [3 ]
Maher, Eamonn R. [2 ]
Kilby, Mark D. [2 ,4 ]
Hurles, Matthew E. [1 ]
机构
[1] Wellcome Trust Sanger Inst, Hinxton CB10 1SA, Cambs, England
[2] Univ Birmingham, Coll Med & Dent Sci, Birmingham Ctr Womens & Childrens Hlth, Sch Clin & Expt Med, Birmingham B15 2TT, W Midlands, England
[3] Birmingham Womens NHS Trust, West Midlands Reg Genet Lab, Birmingham B15 2TG, W Midlands, England
[4] Birmingham Womens Fdn Trust, Fetal Med Ctr, Birmingham B15 2TG, W Midlands, England
基金
英国惠康基金;
关键词
CHROMOSOMAL MICROARRAY; NF1; GENE; MUTATIONS; SPECTRUM; PROTEIN; PHENOTYPE; DISEASE; PAR3;
D O I
10.1093/hmg/ddu038
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The genetic etiology of non-aneuploid fetal structural abnormalities is typically investigated by karyotyping and array-based detection of microscopically detectable rearrangements, and submicroscopic copy-number variants (CNVs), which collectively yield a pathogenic finding in up to 10% of cases. We propose that exome sequencing may substantially increase the identification of underlying etiologies. We performed exome sequencing on a cohort of 30 non-aneuploid fetuses and neonates (along with their parents) with diverse structural abnormalities first identified by prenatal ultrasound. We identified candidate pathogenic variants with a range of inheritance models, and evaluated these in the context of detailed phenotypic information. We identified 35 de novo single-nucleotide variants (SNVs), small indels, deletions or duplications, of which three (accounting for 10% of the cohort) are highly likely to be causative. These are de novo missense variants in FGFR3 and COL2A1, and a de novo 16.8 kb deletion that includes most of OFD1. In five further cases (17%) we identified de novo or inherited recessive or X-linked variants in plausible candidate genes, which require additional validation to determine pathogenicity. Our diagnostic yield of 10% is comparable to, and supplementary to, the diagnostic yield of existing microarray testing for large chromosomal rearrangements and targeted CNV detection. The de novo nature of these events could enable couples to be counseled as to their low recurrence risk. This study outlines the way for a substantial improvement in the diagnostic yield of prenatal genetic abnormalities through the application of next-generation sequencing.
引用
收藏
页码:3269 / 3277
页数:9
相关论文
共 40 条
[1]   Direct Measure of the De Novo Mutation Rate in Autism and Schizophrenia Cohorts [J].
Awadalla, Philip ;
Gauthier, Julie ;
Myers, Rachel A. ;
Casals, Ferran ;
Hamdan, Fadi F. ;
Griffing, Alexander R. ;
Cote, Melanie ;
Henrion, Edouard ;
Spiegelman, Dan ;
Tarabeux, Julien ;
Piton, Amelie ;
Yang, Yan ;
Boyko, Adam ;
Bustamante, Carlos ;
Xiong, Lan ;
Rapoport, Judith L. ;
Addington, Aniene M. ;
DeLisi, J. Lynn E. ;
Krebs, Marie-Odile ;
Joober, Ridha ;
Millet, Bruno ;
Fombonne, Eric ;
Mottron, Laurent ;
Zilversmit, Martine ;
Keebler, Jon ;
Daoud, Hussein ;
Marineau, Claude ;
Roy-Gagnon, Marie-Helene ;
Dube, Marie-Pierre ;
Eyre-Walker, Adam ;
Drapeau, Pierre ;
Stone, Eric A. ;
Lafreniere, Ronald G. ;
Rouleau, Guy A. .
AMERICAN JOURNAL OF HUMAN GENETICS, 2010, 87 (03) :316-324
[2]   Early prenatal ventriculomegaly due to an AIFM1 mutation identified by linkage analysis and whole exome sequencing [J].
Berger, Itai ;
Ben-Neriah, Ziva ;
Dor-Wolman, Talia ;
Shaag, Avraham ;
Saada, Ann ;
Zenvirt, Shamir ;
Raas-Rothschild, Annick ;
Nadjari, Michel ;
Kaestner, Klaus H. ;
Elpeleg, Orly .
MOLECULAR GENETICS AND METABOLISM, 2011, 104 (04) :517-520
[3]   Novel Mutations Including Deletions of the Entire OFD1 Gene in 30 Families with Type 1 Orofaciodigital Syndrome: A Study of the Extensive Clinical Variability [J].
Bisschoff, Izak J. ;
Zeschnigk, Christine ;
Horn, Denise ;
Wellek, Brigitte ;
Riess, Angelika ;
Wessels, Maja ;
Willems, Patrick ;
Jensen, Peter ;
Busche, Andreas ;
Bekkebraten, Jens ;
Chopra, Maya ;
Hove, Hanne Dahlgaard ;
Evers, Christina ;
Heimdal, Ketil ;
Kaiser, Ann-Sophie ;
Kunstmann, Erdmut ;
Robinson, Kristina Lagerstedt ;
Linne, Maja ;
Martin, Patricia ;
McGrath, James ;
Pradel, Winnie ;
Prescott, Katrina E. ;
Roesler, Bernd ;
Rudolf, Gorazd ;
Siebers-Renelt, Ulrike ;
Tyshchenko, Nataliya ;
Wieczorek, Dagmar ;
Wolff, Gerhard ;
Dobyns, William B. ;
Morris-Rosendahl, Deborah J. .
HUMAN MUTATION, 2013, 34 (01) :237-247
[4]   Mutant chromatin remodeling protein SMARCAL1 causes Schimke immuno-osseous dysplasia [J].
Boerkoel, CF ;
Takashima, H ;
John, J ;
Yan, J ;
Stankiewicz, P ;
Rosenbarker, L ;
André, JL ;
Bogdanovic, R ;
Burguet, A ;
Cockfield, S ;
Cordeiro, I ;
Fründ, S ;
Illies, F ;
Joseph, M ;
Kaitila, I ;
Lama, G ;
Loirat, C ;
McLeod, DR ;
Milford, DV ;
Petty, EM ;
Rodrigo, F ;
Saraiva, JM ;
Schmidt, B ;
Smith, GC ;
Spranger, J ;
Stein, A ;
Thiele, H ;
Tizard, J ;
Weksberg, R ;
Lupski, JR ;
Stockton, DW .
NATURE GENETICS, 2002, 30 (02) :215-220
[5]   Prenatal Detection of Aneuploidy and Imbalanced Chromosomal Arrangements by Massively Parallel Sequencing [J].
Dan, Shan ;
Chen, Fang ;
Choy, Kwong Wai ;
Jiang, Fuman ;
Lin, Jingrong ;
Xuan, Zhaoling ;
Wang, Wei ;
Chen, Shengpei ;
Li, Xuchao ;
Jiang, Hui ;
Leung, Tak Yeung ;
Lau, Tze Kin ;
Su, Yue ;
Zhang, Weiyuan ;
Zhang, Xiuqing .
PLOS ONE, 2012, 7 (02)
[6]   Diagnostic Exome Sequencing in Persons with Severe Intellectual Disability [J].
de Ligt, Joep ;
Willemsen, Marjolein H. ;
van Bon, Bregje W. M. ;
Kleefstra, Tjitske ;
Yntema, Helger G. ;
Kroes, Thessa ;
Vulto-van Silfhout, Anneke T. ;
Koolen, David A. ;
de Vries, Petra ;
Gilissen, Christian ;
del Rosario, Marisol ;
Hoischen, Alexander ;
Scheffer, Hans ;
de Vries, Bert B. A. ;
Brunner, Han G. ;
Veltman, Joris A. ;
Vissers, Lisenka E. L. M. .
NEW ENGLAND JOURNAL OF MEDICINE, 2012, 367 (20) :1921-1929
[7]   NF1 gene mutations represent the major molecular event underlying neurofibromatosis-Noonan syndrome [J].
De Luca, A ;
Bottillo, I ;
Sarkozy, A ;
Carta, C ;
Neri, C ;
Bellacchio, E ;
Schirinzi, A ;
Conti, E ;
Zampino, G ;
Battaglia, A ;
Majore, S ;
Rinaldi, MM ;
Carella, M ;
Marino, B ;
Pizzuti, A ;
Digilio, MC ;
Tartaglia, M ;
Dallapiccola, B .
AMERICAN JOURNAL OF HUMAN GENETICS, 2005, 77 (06) :1092-1101
[8]   DLC-1, a Rho GTPase-activating protein with tumor suppressor function, is essential for embryonic development [J].
Durkin, ME ;
Avner, MR ;
Huh, CG ;
Yuan, BZ ;
Thorgeirsson, SS ;
Popescu, NC .
FEBS LETTERS, 2005, 579 (05) :1191-1196
[9]   Mutations in GRIN2A and GRIN2B encoding regulatory subunits of NMDA receptors cause variable neurodevelopmental phenotypes [J].
Endele, Sabine ;
Rosenberger, Georg ;
Geider, Kirsten ;
Popp, Bernt ;
Tamer, Ceyhun ;
Stefanova, Irina ;
Milh, Mathieu ;
Kortuem, Fanny ;
Fritsch, Angela ;
Pientka, Friederike K. ;
Hellenbroich, Yorck ;
Kalscheuer, Vera M. ;
Kohlhase, Juergen ;
Moog, Ute ;
Rappold, Gudrun ;
Rauch, Anita ;
Ropers, Hans-Hilger ;
von Spiczak, Sarah ;
Toennies, Holger ;
Villeneuve, Nathalie ;
Villard, Laurent ;
Zabel, Bernhard ;
Zenker, Martin ;
Laube, Bodo ;
Reis, Andre ;
Wieczorek, Dagmar ;
Van Maldergem, Lionel ;
Kutsche, Kerstin .
NATURE GENETICS, 2010, 42 (11) :1021-U153
[10]   Minor lesion mutational spectrum of the entire NF1 gene does not explain its high mutability but points to a functional domain upstream of the CAP-related domain [J].
Fahsold, R ;
Hoffmeyer, S ;
Mischung, C ;
Gille, C ;
Ehlers, C ;
Kücükceylan, N ;
Abdel-Nour, M ;
Gewies, A ;
Peters, H ;
Kaufmann, D ;
Buske, A ;
Tinschert, S ;
Nürnberg, P .
AMERICAN JOURNAL OF HUMAN GENETICS, 2000, 66 (03) :790-818