A fundamental question related to the formation of organs
is how a developmental field with multiple potential fates is
parsed into regions with a single fate and how boundaries within
these broad developmental fields are established and maintained.
We are addressing these key questions related to organ formation by
dissecting transcription factor networks that control boundary formation
and organ development in vivo using transgenic and knockout mouse
technologies. Current work in the lab is focused on the pathways
controlling the development of the cardiovascular system from the
early embryonic mesoderm, the neural crest into multiple distinct
lineages within the embryo, and skeletal muscle as a model system to
understand transcription factor function. The ultimate goal of these
studies is to understand the basic mechanisms that control normal
organogenesis, how disruptions in these developmental programs result
in congenital defects in humans, and how molecular re-wiring of stem
cells based on normal pathways can ultimately be used therapeutically.
Selected Publications
Liu D, Black BL, Derynck R. 2001. TGF-ß inhibits muscle
differentiation through functional repression
of myogenic transcription factors by Smad3. Genes and Development 15: 2950-2966.
Heidt AB, Black BL. 2005. Transgenic mice that express
Cre recombinase under control of a skeletal muscle-specific promoter from mef2c. Genesis 42: 28-32.
Jaehnig EJ, Heidt AB, Greene SB, Cornelissen I, Black BL. 2006. Increased susceptibility
to isoproterenol-induced cardiac hypertrophy and impaired weight gain in mice
lacking the histidine rich calcium-binding protein. Molecular and Cellular Biology 26: 9315-9326.
Heidt AB, Rojas A, Harris IS, Black BL. 2007. Determinants of myogenic specificity
within MyoD are required for non-canonical E box binding. Molecular and Cellular Biology 27: 5910-5920.
Information last updated September 2007
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