Bernice E Morrow
Albert Einstein College of Medicine, NY·Genetics
Congenital heart disease is the most common type of birth defect, and many cases involve the outflow tract: the part of the embryonic heart that becomes the aorta and pulmonary trunk, the two great arteries leaving the heart. Building it requires two groups of embryonic cells to cooperate.
- Fields
Genetics
Biology
Medicine & Clinical Research
- Topics
congenital heart disease
22q11.2 deletion syndrome
DiGeorge syndrome
- Grants
- 3 known grants, through Apr 2029
What they work on
- Trace the origins and fates of three cardiac neural crest populations (Tbx2/3, Isl1 and Acta2) in mouse embryos using dual lineage tracing, which labels cells and their descendants, and build gene regulatory networks that control their development.
- Test whether neural crest cells in Tbx1-null mouse embryos fail to progress beyond Sox10-expressing progenitors and enter the outflow tract, and how second heart field cells influence this process.
- Identify rare coding, non-coding and structural DNA variants that modify heart defect risk in 22q11.2 deletion syndrome, using whole genomes from 2,577 people and Bayesian prioritization of gene sets from the TBX1 network.
- Validate candidate modifier genes in mouse models and test specific patient DNA variants by gene editing in zebrafish.
- Define how Tbx1 steers multilineage primed progenitors toward heart cell fates, using timed, cell-specific gene deletion with CreERT2 mice plus single-cell RNA-seq, ATAC-seq and spatial transcriptomics.
- Test distant-acting enhancers, DNA switches identified in the omics data, that let Tbx1 regulate cell fate in second heart field cells, using knock-in and knockout mouse transgenesis.
More about the research
Neural crest cells are migrating cells that help form the artery walls. Second heart field cells are a pool of heart-building cells next to the developing heart. A key test case is 22q11.2 deletion syndrome (22q11.2DS, also called DiGeorge syndrome), a disorder caused by a small missing piece of chromosome 22. It affects about 1 in 4,000 births, and roughly 60–70% of patients have heart defects. The lab's projects connect three levels of this problem: how individual embryonic cell types choose their fates in mouse embryos, how the gene TBX1 directs those choices, and which other genes in patients' genomes make heart defects more or less severe.
Why it matters
Many of the genes studied are linked to congenital heart disease in people. Finding genetic modifiers in patients with 22q11.2 deletion syndrome could improve diagnosis and could help explain why some children have severe outflow tract defects, such as tetralogy of Fallot, while others do not. About half of affected patients need surgery to survive. Some of the modifier genes may also be risk factors for heart defects in the general population.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Cell fate choices by Tbx1 in forming the mammalian heart
NIH · Aug 2020 – Apr 2029
Molecular pathogenesis of congenital heart disease mediated by neural crest and second heart field cells
NIH · May 2022 – Apr 2027
Genetic modifiers of congenital heart disease in 22q11.2 deletion syndrome
NIH · Feb 2022 – Jan 2027
Closest labs
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Map where Sox10-expressing taste bud progenitors sit within von Ebner's salivary glands and define their gene signature, using lineage tracing in Sox10-iCreERT2/tdTomato mice and MERFISH imaging of about 140 marker genes.
Anne Nichols
University of Rochester, NY·Physiology·Early-career
Build a spatial and time-course atlas of how GLAST-lineage epitenon progenitors and Scx-expressing tenocytes respond to load. The approach combines genetic lineage tracing in mice with integrated spatial and single-cell RNA sequencing.
Soma Dash
University at Albany, NY·Genetics·Early-career
Identify the mechanism behind craniofacial defects in mice lacking Med23, a Mediator complex subunit, in neural crest cells, by analyzing transcriptomic changes and mapping Med23's DNA and protein binding partners.
The school
Albert Einstein College of Medicine: 21 labs on PI Pages, $361M a year on research, 36 research doctorates a year.
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