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Contact information

Email
duncan.sparrow@dpag.ox.ac.uk

Telephone
01865 272536

Research groups

Sparrow Group

Colleges

Exeter College

Websites

Duncan Sparrow

PhD

Professor of Cardiovascular Developmental Biology

BHF Senior Basic Science Research Fellow
Supernumerary Fellow of Exeter College

Duncan Sparrow completed his PhD at the University of Adelaide in the field of the regulation of tissue-specific transcription. He moved to the National Institute for Medical Research in Mill Hill for his first postdoc, where he worked with Dr Tim Mohun on the developmental biology of heart and skeletal muscle formation in Xenopus laevis. He then returned to Australia to take up the position of Senior Research Scientist in Professor Sally Dunwoodie's laboratory at the Victor Chang Cardiac Research Institute. There he investigated the genetic and environmental causes of congenital vertebral malformation in human patients and mouse models.

His current research focus is how embryonic heart development can be perturbed by both genetic and environmental means. He is supported by funding from the British Heart Foundation, Additional Ventures, The John Fell Fund and the Federated Foundation.

Key publications

Maternal anaemia and congenital heart disease in offspring: a case-control study using linked electronic health records in the United Kingdom

Nair M. et al, (2025), BJOG: An International Journal of Obstetrics and Gynaecology

Maternal iron deficiency perturbs embryonic cardiovascular development in mice.

Kalisch-Smith JI. et al, (2021), Nature communications, 12

Environmental Risk Factors for Congenital Heart Disease

Kalisch-Smith JI. et al, (2019), Cold Spring Harbor Perspectives in Biology, a037234 - a037234

NAD Deficiency, Congenital Malformations and Niacin Supplementation

Shi H. et al, (2017), New England Journal of Medicine

Gestational Stress Induces the Unfolded Protein Response Resulting in Heart Defects

Shi H. et al, (2016), Development

mechanism for gene-environment interaction in the etiology of congenital scoliosis.

Sparrow DB. et al, (2012), Cell, 149, 295 - 306

Recent publications

Distinct roles of the Lyve1 lineage in heart development

Klaourakis K. et al, (2026)

Maternal anaemia and congenital heart disease in offspring: a case-control study using linked electronic health records in the United Kingdom

Nair M. et al, (2025), BJOG: An International Journal of Obstetrics and Gynaecology

Maternal anaemia during pregnancy is associated with an increase in the risk of offspring congenital heart disease: a case-control study using linked electronic health records in England

Nair M. et al, (2024)

Noncoding regulation of epicardial gene expression and epithelial-to-mesenchymal transition during heart development

Vieira JN. et al, (2024), CIRCULATION RESEARCH, 135

Insights into the Role of a Cardiomyopathy-Causing Genetic Variant in ACTN2

Broadway-Stringer S. et al, (2023), Cells

Better communication between experts is needed to solve the environmental origins of birth defects.

Sparrow DB., (2022), Bioessays, 44

nalysis of Placental Arteriovenous Formation Reveals New Insights Into Embryos With Congenital Heart Defects

KALISCH-SMITH J. et al, (2022), Frontiers in Genetics

Myhre syndrome is caused by dominant-negative dysregulation of SMAD4 and other co-factors.

Alankarage D. et al, (2022), Differentiation, 128, 1 - 12

Small change, big impact: A Z-disc missense genetic variant causes dramatic morphological changes in the embryonic heart

Jiang H. et al, (2022), JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 173, S44 - S44

The onset of circulation triggers a metabolic switch required for endothelial to hematopoietic transition.

Azzoni E. et al, (2021), Cell Rep, 37

Maternal iron deficiency perturbs embryonic cardiovascular development in mice.

Kalisch-Smith JI. et al, (2021), Nature communications, 12

Maternal iron deficiency perturbs embryonic cardiovascular development in mice

SPARROW D. et al, (2021), Nature Communications

Functional analysis of a gene-edited mouse to gain insights into the disease mechanisms of a titin missense variant

JIANG H. et al, (2021), Basic Research in Cardiology

Maternal iron deficiency impacts the placental arterial network

Kalisch-Smith J. et al, (2021)

Heterozygous loss of WBP11 function causes multiple congenital defects in humans and mice

Martin E. et al, (2020), Human Molecular Genetics

Functional genomics and gene-environment interaction highlight the complexity of Congenital Heart Disease caused by Notch pathway variants

Chapman G. et al, (2019), Human Molecular Genetics

Environmental Risk Factors for Congenital Heart Disease

Kalisch-Smith JI. et al, (2019), Cold Spring Harbor Perspectives in Biology, a037234 - a037234

Tamoxifen administration in pregnant mice can be deleterious to both mother and embryo

VED N. et al, (2019), Laboratory Animals

Gene-environment interaction impacts on heart development and embryo survival

Moreau JLM. et al, (2019), Development, 146, dev172957 - dev172957

Screening Approach to Identify Clinically Actionable Variants Causing Congenital Heart Disease in Exome Data

Szot JO. et al, (2018), Circulation: Genomic and Precision Medicine

NAD Deficiency, Congenital Malformations and Niacin Supplementation

Shi H. et al, (2017), New England Journal of Medicine

Gestational stress induces the unfolded protein response, resulting in heart defects

Moreau JLM. et al, (2017), MECHANISMS OF DEVELOPMENT, 145, S67 - S68

Gestational Stress Induces the Unfolded Protein Response Resulting in Heart Defects

Shi H. et al, (2016), Development

Renal developmental defects resulting from in utero hypoxia are associated with suppression of ureteric β-catenin signaling.

Wilkinson LJ. et al, (2015), Kidney Int, 87, 975 - 983

Compound heterozygous mutations in RIPPLY2 associated with vertebral segmentation defects.

McInerney-Leo AM. et al, (2015), Hum Mol Genet, 24, 1234 - 1242

Genetic and Environmental Interaction in Malformation of the Vertebral Column

Dunwoodie SL. and Sparrow DB., (2015)

Cited2 is required in trophoblasts for correct placental capillary patterning.

Moreau JLM. et al, (2014), Dev Biol, 392, 62 - 79

Gene-environment interaction demonstrates the vulnerability of the embryonic heart.

O'Reilly VC. et al, (2014), Dev Biol, 391, 99 - 110

Mutation of HES7 in a large extended family with spondylocostal dysostosis and dextrocardia with situs inversus.

Sparrow DB. et al, (2013), Am J Med Genet A, 161A, 2244 - 2249

somal dominant spondylocostal dysostosis is caused by mutation in TBX6.

Sparrow DB. et al, (2013), Hum Mol Genet, 22, 1625 - 1631

mechanism for gene-environment interaction in the etiology of congenital scoliosis.

Sparrow DB. et al, (2012), Cell, 149, 295 - 306

The mouse notches up another success: understanding the causes of human vertebral malformation.

Sparrow DB. et al, (2011), Mamm Genome, 22, 362 - 376

Loss of Cited2 causes congenital heart disease by perturbing left-right patterning of the body axis.

Lopes Floro K. et al, (2011), Hum Mol Genet, 20, 1097 - 1110

Notch inhibition by the ligand DELTA-LIKE 3 defines the mechanism of abnormal vertebral segmentation in spondylocostal dysostosis.

Chapman G. et al, (2011), Hum Mol Genet, 20, 905 - 916

Complex SUMO-1 regulation of cardiac transcription factor Nkx2-5.

Costa MW. et al, (2011), PLoS One, 6

somal dominant spondylocostal dysostosis in three generations of a Macedonian family: Negative mutation analysis of DLL3, MESP2, HES7, and LFNG.

Gucev ZS. et al, (2010), Am J Med Genet A, 152A, 1378 - 1382

Two novel missense mutations in HAIRY-AND-ENHANCER-OF-SPLIT-7 in a family with spondylocostal dysostosis.

Sparrow DB. et al, (2010), Eur J Hum Genet, 18, 674 - 679

Cyclical expression of the Notch/Wnt regulator Nrarp requires modulation by Dll3 in somitogenesis.

Sewell W. et al, (2009), Dev Biol, 329, 400 - 409

Placental insufficiency associated with loss of Cited1 causes renal medullary dysplasia.

Sparrow DB. et al, (2009), J Am Soc Nephrol, 20, 777 - 786

Mutation of Hairy-and-Enhancer-of-Split-7 in humans causes spondylocostal dysostosis.

Sparrow DB. et al, (2008), Hum Mol Genet, 17, 3761 - 3766

BMP/SMAD1 signaling sets a threshold for the left/right pathway in lateral plate mesoderm and limits availability of SMAD4.

Furtado MB. et al, (2008), Genes Dev, 22, 3037 - 3049

Old Wares and New: Five Decades of Investigation of Somitogenesis in Xenopus laevis

Sparrow DB., (2008), 638, 73 - 94

Spondylocostal dysostosis in a pregnancy complicated by confined placental mosaicism for tetrasomy 9p.

Coman D. et al, (2008), Am J Med Genet A, 146A, 1972 - 1976

SmcHD1, containing a structural-maintenance-of-chromosomes hinge domain, has a critical role in X inactivation.

Blewitt ME. et al, (2008), Nat Genet, 40, 663 - 669

Divergent functions and distinct localization of the Notch ligands DLL1 and DLL3 in vivo.

Geffers I. et al, (2007), J Cell Biol, 178, 465 - 476

Disruption of the somitic molecular clock causes abnormal vertebral segmentation.

Sparrow DB. et al, (2007), Birth Defects Res C Embryo Today, 81, 93 - 110

The transcriptional activity of CITED1 is regulated by phosphorylation in a cell cycle-dependent manner.

Shi G. et al, (2006), J Biol Chem, 281, 27426 - 27435

Loss of Cited2 affects trophoblast formation and vascularization of the mouse placenta.

Withington SL. et al, (2006), Dev Biol, 294, 67 - 82

Generation of conditional Cited2 null alleles

Preis JI. et al, (2006), Genesis, 44, 579 - 583

Xenopus laevis transgenesis by sperm nuclear injection.

Smith SJ. et al, (2006), Nat Protoc, 1, 2195 - 2203

Mutation of the LUNATIC FRINGE gene in humans causes spondylocostal dysostosis with a severe vertebral phenotype.

Sparrow DB. et al, (2006), Am J Hum Genet, 78, 28 - 37

Evolution of distinct EGF domains with specific functions.

Wouters MA. et al, (2005), Protein Sci, 14, 1091 - 1103

The MLC1v gene provides a transgenic marker of myocardium formation within developing chambers of the Xenopus heart.

Smith SJ. et al, (2005), Dev Dyn, 232, 1003 - 1012

Mutated MESP2 causes spondylocostal dysostosis in humans.

Whittock NV. et al, (2004), Am J Hum Genet, 74, 1249 - 1254

Transcriptional regulation of the cardiac-specific MLC2 gene during Xenopus embryonic development.

Latinkic BV. et al, (2004), Development, 131, 669 - 679

Kousseff syndrome: a causally heterogeneous disorder.

Maclean K. et al, (2004), Am J Med Genet A, 124A, 307 - 312

Cited1 is required in trophoblasts for placental development and for embryo growth and survival.

Rodriguez TA. et al, (2004), Mol Cell Biol, 24, 228 - 244

Kousseff syndrome: A causally heterogeneous disorder

Maclean K. et al, (2004), AMERICAN JOURNAL OF MEDICAL GENETICS PART A, 124A, 307 - 312

Distinct enhancers regulate skeletal and cardiac muscle-specific expression programs of the cardiac alpha-actin gene in Xenopus embryos.

Latinkić BV. et al, (2002), Dev Biol, 245, 57 - 70

Diverse requirements for Notch signalling in mammals

Sparrow DB. et al, (2002), The International Journal of Developmental Biology, 46, 365 - 374

xial skeletal defects caused by mutation in the spondylocostal dysplasia/pudgy gene Dll3 are associated with disruption of the segmentation clock within the presomitic mesoderm

Dunwoodie SL. et al, (2002), Development, 129, 1795 - 1806

Diverse requirements for Notch signalling in mammals

Sparrow DB. et al, (2002), INTERNATIONAL JOURNAL OF DEVELOPMENTAL BIOLOGY, 46, 365 - 374

The small muscle-specific protein Csl modifies cell shape and promotes myocyte fusion in an insulin-like growth factor 1-dependent manner.

Palmer S. et al, (2001), J Cell Biol, 153, 985 - 998

Regulation of the tinman homologues in Xenopus embryos.

Sparrow DB. et al, (2000), Dev Biol, 227, 65 - 79

simplified method of generating transgenic Xenopus.

Sparrow DB. et al, (2000), Nucleic Acids Res, 28

Subdivision of the cardiac Nkx2.5 expression domain into myogenic and nonmyogenic compartments.

Raffin M. et al, (2000), Dev Biol, 218, 326 - 340

The morphology of heart development in Xenopus laevis.

Mohun TJ. et al, (2000), Dev Biol, 218, 74 - 88

MEF-2 function is modified by a novel co-repressor, MITR.

Sparrow DB. et al, (1999), EMBO J, 18, 5085 - 5098

Heart developmental biology. Introduction

Mohun TJ. and Sparrow DB., (1999), Seminars in Cell and Developmental Biology, 10, 59 - 60

Xenopus eHAND: a marker for the developing cardiovascular system of the embryo that is regulated by bone morphogenetic proteins.

Sparrow DB. et al, (1998), Mech Dev, 71, 151 - 163

Thylacine 1 is expressed segmentally within the paraxial mesoderm of the Xenopus embryo and interacts with the Notch pathway

Sparrow DB. et al, (1998), Development, 125, 2041 - 2051

Ubc9p and the conjugation of SUMO-1 to RanGAP1 and RanBP2

Saitoh H. et al, (1998), Current Biology, 8, 121 - 124

Early steps in vertebrate cardiogenesis.

Mohun T. and Sparrow D., (1997), Curr Opin Genet Dev, 7, 628 - 633

MEF2 proteins, including MEF2A, are expressed in both muscle and non-muscle cells.

Dodou E. et al, (1995), Nucleic Acids Res, 23, 4267 - 4274

ntigenic and genetic characterization of current influenza strains.

Hay AJ. et al, (1994), Eur J Epidemiol, 10, 465 - 466

The RSRF/MEF2 protein SL1 regulates cardiac muscle-specific transcription of a myosin light-chain gene in Xenopus embryos.

Chambers AE. et al, (1994), Genes Dev, 8, 1324 - 1334

Sequence of a cDNA encoding chicken high-mobility-group protein-2.

Sparrow DB. and Wells JR., (1992), Gene, 114, 289 - 290

Sequence of a cDNA encoding chicken high-mobility-group protein-2

Sparrow DB. and Wells JRE., (1992), Gene, 114, 289 - 290

More publications