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1. The many faces of the Wall

Author

Woodward, Geoff, primary, Savage, Joe, additional, Claxton, Kiki, additional, Poad, Andrew, additional, Laskey, Jane, additional, Breeze, David J., additional, Aglionby, Susan, additional, and Richards, Mark, additional

Published
2022
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2. Expanding the clinical spectrum of recessive truncating mutations of KLHL7 to a Bohring-Opitz-like phenotype

Author

Bruel, Ange-Line, Bigoni, Stefania, Kennedy, Joanna, Whiteford, Margo, Buxton, Chris, Parmeggiani, Giulia, Wherlock, Matt, Woodward, Geoff, Greenslade, Mark, Williams, Maggie, St-Onge, Judith, Ferlini, Alessandra, Garani, Giampaolo, Ballardini, Elisa, van Bon, Bregje W, Acuna-Hidalgo, Rocio, Bohring, Axel, Deleuze, Jean-François, Boland, Anne, Meyer, Vincent, Olaso, Robert, Ginglinger, Emmanuelle, Study, DDD, Rivière, Jean-Baptiste, Brunner, Han G, Hoischen, Alexander, Newbury-Ecob, Ruth, Faivre, Laurence, Thauvin-Robinet, Christel, and Thevenon, Julien

Published
2017
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5. Prenatal exposure to maternal cigarette smoking and DNA methylation: epigenome-wide association in a discovery sample of adolescents and replication in an independent cohort at birth through 17 years of age

Author

Lee, Ken W.K., Richmond, Rebecca, Hu, Pingzhao, French, Leon, Shin, Jean, Bourdon, Celine, Reischl, Eva, Waldenberger, Melanie, Zeilinger, Sonja, Gaunt, Tom, McArdle, Wendy, Ring, Susan, Woodward, Geoff, Bouchard, Luigi, Gaudet, Daniel, Smith, George Davey, Relton, Caroline, Paus, Tomas, and Pausova, Zdenka

Subjects
DNA -- Physiological aspects -- Research, Methylation -- Research, Smoking in pregnancy -- Health aspects -- Research, Environmental issues, Health
Abstract

BACKGROUND: Prenatal exposure to maternal cigarette smoking (prenatal smoke exposure) had been associated with altered DNA methylation (DNAm) at birth. OBJECTIVE: We examined whether such alterations are present from birth through adolescence. METHODS: We used the Infinium Human Methylation 450K BeadChip to search across 473,395 CpGs for differential DNAm associated with prenatal smoke exposure during adolescence in a discovery cohort (n = 132) and at birth, during childhood, and during adolescence in a replication cohort (n = 447). RESULTS: In the discovery cohort, we found five CpGs in MYO1G (top-ranking CpG: cg12803068, p = 3.3 x [10.sup.-11]) and CNTNAP2 (cg25949550, p = 4.0 x [10.sup.-9]) to be differentially methylated between exposed and nonexposed individuals during adolescence. The CpGs in MYO1G and CNTNAP2 were associated, respectively, with higher and lower DNAm in exposed versus nonexposed adolescents. The same CpGs were differentially methylated at birth, during childhood, and during adolescence in the replication cohort. In both cohorts and at all developmental time points, the differential DNAm was in the same direction and of a similar magnitude, and was not altered appreciably by adjustment for current smoking by the participants or their parents. In addition, four of the five EWAS (epigenome-wide association study)--significant CpGs in the adolescent discovery cohort were also among the top sites of differential methylation in a previous birth cohort, and differential methylation of CpGs in CYP1A1, AHRR, and GFI1 observed in that study was also evident in our discovery cohort. CONCLUSIONS: Our findings suggest that modifications of DNAm associated with prenatal maternal smoking may persist in exposed offspring for many years--at least until adolescence. citation: Lee KW, Richmond R, Hu P, French L, Shin J, Bourdon C, Reischl E, Waldenberger M, ZeilingerS, Gaunt T, McArdle W, Ring S, Woodward G, Bouchard L, GaudetD, Davey Smith G, Relton C, Paus T, Pausova Z. 2015. Prenatal exposure to maternal cigarette smoking and DNA methylation: epigenome-wide association in a discovery sample of adolescents and replication in an independent cohort at birth through 17 years of age. Environ Health Perspect 123:193-199; http://dx.doi.org/10.1289/ehp.1408614, Introduction Maternal cigarette smoking during pregnancy was and still is common in the industrialized world. In the United States, for example, 30-40% of pregnant women smoked in the 1960s and [...]

Published
2015
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6. Prenatal exposure to maternal smoking and offspring DNA methylation across the lifecourse: findings from the Avon Longitudinal Study of Parents and Children (ALSPAC)

Author

Richmond, Rebecca C., Simpkin, Andrew J., Woodward, Geoff, Gaunt, Tom R., Lyttleton, Oliver, McArdle, Wendy L., Ring, Susan M., Smith, Andrew D.A.C., Timpson, Nicholas J., Tilling, Kate, Davey Smith, George, and Relton, Caroline L.

Subjects
Male, Adolescent, Smoking, Infant, Newborn, Infant, Articles, DNA Methylation, Pedigree, Cohort Studies, Maternal Exposure, Pregnancy, Prenatal Exposure Delayed Effects, Humans, Female, Longitudinal Studies, Child
Abstract

Maternal smoking during pregnancy has been found to influence newborn DNA methylation in genes involved in fundamental developmental processes. It is pertinent to understand the degree to which the offspring methylome is sensitive to the intensity and duration of prenatal smoking. An investigation of the persistence of offspring methylation associated with maternal smoking and the relative roles of the intrauterine and postnatal environment is also warranted. In the Avon Longitudinal Study of Parents and Children, we investigated associations between prenatal exposure to maternal smoking and offspring DNA methylation at multiple time points in approximately 800 mother-offspring pairs. In cord blood, methylation at 15 CpG sites in seven gene regions (AHRR, MYO1G, GFI1, CYP1A1, CNTNAP2, KLF13 and ATP9A) was associated with maternal smoking, and a dose-dependent response was observed in relation to smoking duration and intensity. Longitudinal analysis of blood DNA methylation in serial samples at birth, age 7 and 17 years demonstrated that some CpG sites showed reversibility of methylation (GFI1, KLF13 and ATP9A), whereas others showed persistently perturbed patterns (AHRR, MYO1G, CYP1A1 and CNTNAP2). Of those showing persistence, we explored the effect of postnatal smoke exposure and found that the major contribution to altered methylation was attributed to a critical window of in utero exposure. A comparison of paternal and maternal smoking and offspring methylation showed consistently stronger maternal associations, providing further evidence for causal intrauterine mechanisms. These findings emphasize the sensitivity of the methylome to maternal smoking during early development and the long-term impact of such exposure.

Published
2014

7. Expanding the clinical spectrum of recessive truncating mutations ofKLHL7to a Bohring-Opitz-like phenotype

Author

Bruel, Ange-Line, primary, Bigoni, Stefania, additional, Kennedy, Joanna, additional, Whiteford, Margo, additional, Buxton, Chris, additional, Parmeggiani, Giulia, additional, Wherlock, Matt, additional, Woodward, Geoff, additional, Greenslade, Mark, additional, Williams, Maggie, additional, St-Onge, Judith, additional, Ferlini, Alessandra, additional, Garani, Giampaolo, additional, Ballardini, Elisa, additional, van Bon, Bregje W, additional, Acuna-Hidalgo, Rocio, additional, Bohring, Axel, additional, Deleuze, Jean-François, additional, Boland, Anne, additional, Meyer, Vincent, additional, Olaso, Robert, additional, Ginglinger, Emmanuelle, additional, Study, DDD, additional, Rivière, Jean-Baptiste, additional, Brunner, Han G, additional, Hoischen, Alexander, additional, Newbury-Ecob, Ruth, additional, Faivre, Laurence, additional, Thauvin-Robinet, Christel, additional, and Thevenon, Julien, additional

Published
2017
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8. 210 Clinical Utility of Gene Panel and Clinical Exome Testing in Cardiac Disease

Author

Gable, Mary, primary, Buxton, Chris, additional, Woodward, Geoff, additional, Wadsley, Marc, additional, Honeychurch, Julie, additional, Joanne, Davies, additional, Newbury-Ecob, Ruth, additional, Low, Karen, additional, Donaldson, Alan, additional, Affleck, Josphine, additional, Whittington, Rebecca, additional, Greenslade, Mark, additional, and Williams, Maggie, additional

Published
2016
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9. Systematic identification of genetic influences on methylation across the human life course

Author

Gaunt, Tom R., primary, Shihab, Hashem A., additional, Hemani, Gibran, additional, Min, Josine L., additional, Woodward, Geoff, additional, Lyttleton, Oliver, additional, Zheng, Jie, additional, Duggirala, Aparna, additional, McArdle, Wendy L., additional, Ho, Karen, additional, Ring, Susan M., additional, Evans, David M., additional, Davey Smith, George, additional, and Relton, Caroline L., additional

Published
2016
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10. Data Resource Profile: Accessible Resource for Integrated Epigenomic Studies (ARIES)

Author

Relton, Caroline L, primary, Gaunt, Tom, additional, McArdle, Wendy, additional, Ho, Karen, additional, Duggirala, Aparna, additional, Shihab, Hashem, additional, Woodward, Geoff, additional, Lyttleton, Oliver, additional, Evans, David M, additional, Reik, Wolf, additional, Paul, Yu-Lee, additional, Ficz, Gabriella, additional, Ozanne, Susan E, additional, Wipat, Anil, additional, Flanagan, Keith, additional, Lister, Allyson, additional, Heijmans, Bastiaan T, additional, Ring, Susan M, additional, and Davey Smith, George, additional

Published
2015
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11. Expanding the clinical spectrum of recessive truncating mutations of KLHL7to a Bohring-Opitz-like phenotype

Author

Bruel, Ange-Line, Bigoni, Stefania, Kennedy, Joanna, Whiteford, Margo, Buxton, Chris, Parmeggiani, Giulia, Wherlock, Matt, Woodward, Geoff, Greenslade, Mark, Williams, Maggie, St-Onge, Judith, Ferlini, Alessandra, Garani, Giampaolo, Ballardini, Elisa, van Bon, Bregje W, Acuna-Hidalgo, Rocio, Bohring, Axel, Deleuze, Jean-Francois, Boland, Anne, Meyer, Vincent, Olaso, Robert, Ginglinger, Emmanuelle, Study, DDD, Rivière, Jean-Baptiste, Brunner, Han G, Hoischen, Alexander, Newbury-Ecob, Ruth, Faivre, Laurence, Thauvin-Robinet, Christel, and Thevenon, Julien

Abstract

BackgroundBohring-Opitz syndrome (BOS) is a rare genetic disorder characterised by a recognisable craniofacial appearance and a typical ‘BOS’ posture. BOS is caused by sporadic mutations ofASXL1. However, several typical patients with BOS have no molecular diagnosis, suggesting clinical and genetic heterogeneity.ObjectivesTo expand the phenotypical spectrum of autosomal recessive variants of KLHL7, reported as causing Crisponi syndrome/cold-induced sweating syndrome type 1 (CS/CISS1)-like syndrome.MethodsWe performed whole-exome sequencing in two families with a suspected recessive mode of inheritance. We used the Matchmaker Exchange initiative to identify additional patients.ResultsHere, we report six patients with microcephaly, facial dysmorphism, including exophthalmos, nevus flammeus of the glabella and joint contractures with a suspected BOS posture in five out of six patients. We identified autosomal recessive truncating mutations in the KLHL7gene. KLHL7encodes a BTB–kelch protein implicated in the cell cycle and in protein degradation by the ubiquitin–proteasome pathway. Recently, biallelic mutations in the KLHL7gene were reported in four families and associated with CS/CISS1, characterised by clinical features overlapping with our patients.ConclusionWe have expanded the clinical spectrum of KLHL7autosomal recessive variants by describing a syndrome with features overlapping CS/CISS1 and BOS.

Published
2017
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13. Panel discussion

Author

Ehlers, Niels, primary, Kersley, H. Johnathan, additional, Tomlinson, Alan, additional, Woodward, Geoff, additional, Efron, Nathan, additional, and McMonnies, Charles, additional

Published
1991
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15. WHAT YOU'RE SAYING.

Author

Ng, David, Baldwin, Stephen, Bard, Liam, Stockely, Marian, Hood, Christian, Jones, Brendan, Colbright, Jenny, Woodward, Geoff, and Mayer, Andy

Published
2020

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