Faculty Profile

Montefiore Einstein Home
Albert Einstein College of Medicine
Faculty Directory
Bernice E. Morrow, Ph.D.

Bernice E. Morrow, Ph.D.

Professor, Department of Genetics

Professor, Department of Obstetrics & Gynecology and Women's Health

Professor, Department of Pediatrics (Pediatric Cardiology)

Sidney L. and Miriam K. Olson Chair in Cardiology

Director, Department of Genetics Division of Translational Genetics

Faculty Advisor, Department of Genetics Genomics Core

Area of Research: The main areas of research include human genetics and mammalian embryonic development. We are taking functional genomic and epigenomic approaches on a single cell level to understand the cause of birth defects.

Contact Information

718.678.1121bernice.morrow@einsteinmed.edu

Albert Einstein College of Medicine
Michael F. Price Center
1301 Morris Park Avenue, Room 402
Bronx, NY 10461

Research Profiles Einstein Media Expert PubMed Portal

More Resources: Division of Translational Genetics

Is this your profile? Edit profile

Professional Interests

Our lab is interested in the mechanisms responsible for birth defects in humans. For this, we are investigating a genetic condition termed 22q11.2 deletion syndrome (22q11.2DS). Patients have a 3 million base pair deletion of one copy of chromosome 22q11.2. Most patients are affected with intellectual disability, congenital heart disease and other malformations, occurring at varied severity. To understand the reasons for varied severity, we are analyzing whole genome sequence from human subjects with 22q11.2DS to identify genetic modifiers. We recruited human subjects internationally and also through the new Montefiore-Einstein Regional Center for 22q11.2DS. Our hypothesis is that genes acting in the same genetic pathway as the deleted genes, act as modifiers of phenotypes. We are taking a candidate gene approach in which genes have been chosen from functional studies of mouse models of 22q11.2DS.

We are investigating the function of three genes, TBX1, DGCR8 and CRKL in mouse models. These genes are deleted in the 22q11.2 region. TBX1 encodes a T-box transcription factor, DGCR8 encodes a microRNA processor and CRKL encodes a cytoplasmic adaptor protein. Inactivation of either results in congenital heart defects in mice. We are taking functional genomic and epigenomic approaches on a single cell level to understand the connections to disease. For TBX1, we identified a progenitor cell population that is required for cell fate transitions in heart development. For DGCR8, we are investigating canonical and non-canonical microRNA functions. For CRKL, we are studying its role in neural crest cells in mediating cell signaling required for heart development. Finally, we are investigating TBX1, TBX2 and TBX3 in inner ear development in embryogenesis.

Selected Publications

Racedo SE, Hasten E, Lin M, Devakanmalai GS, Guo T, Ozbudak EM, Cai C, Zheng D, Morrow BE. (2017) PLoS Genet. 2017;13(3):e1006687. PMID: 28346476 PMCID: PMC5386301

Morrow BE, McDonald-McGinn DM, Emanuel BS, Vermeesch JR, Scambler PJ. (2018) Molecular genetics of 22q11.2 deletion syndrome. Am J Med Genet A. 176(10):2070-2081. PMID: 30380194; PMCID: PMC6214629

Hasten E, Morrow BE. (2019) Tbx1 and Foxi3 genetically interact in the pharyngeal pouch endoderm in a mouse model for 22q11.2 deletion syndrome. PLoS Genet. 15(8):e1008301. PMID: 31412026; PMCID: PMC6709926.

ZhaoY, Diacou A, J......MorrowBE. (2020) Complete sequence of the 22q11.2 allele in 1,053 subjects with 22q11.2 deletion syndrome reveals modifiers of conotruncal heart defects. Am J Hum Genet. 106(1):26-40. PMID: 31870554

Quick Links

Faculty Profile

Bernice E. Morrow, Ph.D.

Contact Information

Professional Interests

Selected Publications

Related News

Research Brief

Studying the Molecular Mechanisms Underlying Congenital Heart Disease

Research Brief

Getting to the Heart of 22q11.2 Deletion Syndrome

Research Brief

Finding the Causes of Congenital Heart Disease

Research Brief

Understanding Heart Malformations