- PROFESSOR | Cell, Developmental & Regenerative Biology
- PROFESSOR | Oncological Sciences
For more information, please visit the Krauss Laboratory website.
Cell Adhesion, Cell Biology, Cellular Differentiation, Cytoskeleton, Developmental Biology, Developmental Neurobiology, Genetics, Human Genetics and Genetic Disorders, Knockout Mice, Muscle Cells, Muscular Dystrophy, Protein Kinases, Signal Transduction, Stem Cells
Multi-Disciplinary Training Areas
Cancer Biology [CAB], Developmental and Stem Cell Biology [DSCB]
PhD, University of North Carolina
Postdoc, Columbia University
Molecular and Cellular Biology
Society for Muscle Biology
Journal of Cell Science
Established Investigator Award
American Heart Association
Career Scientist Award
Irma T. Hirschl Trust
The Krauss lab is interested in regulation of cell adhesion and signal transduction pathways during embryonic development and tissue regeneration, and how such processes may go awry in disease. The lab has two major areas of focus.
First, we are interested in development and regeneration of skeletal muscle. We have identified multiprotein cell surface complexes that promote differentiation of skeletal muscle precursor cells in response to cell-cell contact and adhesion. We use a combination of approaches, including mouse genetics, cell biology and biochemistry to probe the biological functions and molecular mechanisms of such complexes in skeletal myogenesis. We have recently turned our attention to how specific cell adhesion molecules regulate the niche and activity of muscle stem cells during homeostasis and regeneration following injury.
We are also interested mechanisms whereby the Hedgehog signaling pathway regulates development of the midline of the forebrain and midface. Mutations in Hedgehog pathway genes are associated with the common and often devastating developmental defect holoprosencephaly (HPE). However, the clinical outcome of mutation carriers is extremely variable, and additional genetic or environmental factors are required for strong defects. Using mouse models of such interactions and functional analyses of human HPE-associated mutations, we aim to provide information on mechanisms of HPE that will be valuable for genetic counseling and preventive action.
For more information, please visit the Krauss Laboratory website.
Hong M, Srivastava K, Kim S, Allen BL, Leahy DJ, Hu P, Roessler E, Krauss RS, Muenke M. BOC is a modifier gene in holoprosencephaly. Human mutation 2017 Jul;.
Hong M, Krauss RS. Ethanol itself is a holoprosencephaly-inducing teratogen. PloS one 2017 Apr; 12(4).
Joseph GA, Lu M, Radu M, Lee JK, Burden SJ, Chernoff J, Krauss RS. Group I Paks Promote Skeletal Myoblast Differentiation In Vivo and In Vitro. Molecular and cellular biology 2017 Feb; 37(4).
Krauss RS, Joseph GA, Goel AJ. Keep Your Friends Close: Cell-Cell Contact and Skeletal Myogenesis. Cold Spring Harbor perspectives in biology 2017 Feb; 9(2).
Kahn BM, Corman TS, Lovelace K, Hong M, Krauss RS, Epstein DJ. Prenatal ethanol exposure in mice phenocopies Cdon mutation by impeding Shh function in the etiology of optic nerve hypoplasia. Disease models & mechanisms 2017 Jan; 10(1).
Shin JY, Méndez-López I, Hong M, Wang Y, Tanji K, Wu W, Shugol L, Krauss RS, Dauer WT, Worman HJ. Lamina-associated polypeptide 1 is dispensable for embryonic myogenesis but required for postnatal skeletal muscle growth. Human molecular genetics 2017 Jan; 26(1).
Krauss RS, Chihara D, Romer AI. Embracing change: striated-for-smooth muscle replacement in esophagus development. Skeletal muscle 2016 Aug; 6.
Krauss RS, Hong M. Gene-Environment Interactions and the Etiology of Birth Defects. Current topics in developmental biology 2016 Feb; 116.
Chihara D, Romer AI, Bentzinger CF, Rudnicki MA, Krauss RS. PAX7 is required for patterning the esophageal musculature. Skeletal muscle 2015 Dec; 5.
Lee HJ, Jo SB, Romer AI, Lim HJ, Kim MJ, Koo SH, Krauss RS, Kang JS. Overweight in mice and enhanced adipogenesis in vitro are associated with lack of the Hedgehog coreceptor Boc. Diabetes 2015 Jun; 64: 2092-2103.
Hong M, Krauss RS. Rescue of holoprosencephaly in fetal alcohol-exposed Cdon mutant mice by reduced gene dosage of Ptch1. PLOS ONE 2013; 8(11): e79269.
Romer AI, Singh J, Rattan S, Krauss RS. Smooth muscle fascicular reorientation is required for esophageal morphogenesis and dependent on Cdo. J. Cell Biol. 2013; 201: 309-323.
Hong M, Krauss RS. Cdon mutation and fetal ethanol exposure synergize to produce midline signaling defects and holoprosencephaly spectrum disorders in mice. PLoS Genet. 2012; 8(10): e1002999.
Bae GU, Domené S, Roessler E, Schachter K, Kang JS, Muenke M, Krauss RS. Mutations in CDON, encoding a hedgehog receptor, result in holoprosencephaly and defective interactions with other hedgehog receptors. Amer. J. Hum. Genet. 2011; 89: 231-240.
Allen BL, Song JY, Izzi L, Althaus IW, Kang JS, Charron F, Krauss RS, McMahon AP. Overlapping roles and collective requirement for the co-receptors Gas1, Cdo and Boc in Shh pathway function. Dev Cell 2011; 20: 775-787.
Zhang W, Hong M, Bae GU, Kang JS, Krauss RS. Boc modifies the holoprosencephaly spectrum of Cdo mutant mice. Dis Model Mech 2011; 4: 368-380.
Lu M, Krauss RS. N-cadherin ligation, but not Sonic hedgehog binding, initiates Cdo-dependent p38α/β MAPK signaling in skeletal myoblasts. Proc. Natl. Acad. Sci. (USA) 2010; 107: 4212-4217.
Bae GU, Yang YJ, Jiang G, Hong M, Lee HJ, Tessier-Lavigne M, Kang JS, Krauss RS. The Ig superfamily member neogenin regulates myofiber size and focal adhesion kinase and extracellular signal-regulated kinase activities in vivo and in vitro. Mol. Biol. Cell 2009; 20: 4920-4931.
Kang JS, Bae GU, Yi MJ, Yang YJ, Oh JE, Takaesu G, Zhou YT, Low BC, Krauss RS. A Cdo/Bnip-2/Cdc42 signaling pathway regulates p38α/β MAPK activity and myogenic differentiation. J. Cell Biol. 2008; 182: 497-507.
Physicians and scientists on the faculty of the Icahn School of Medicine at Mount Sinai often interact with pharmaceutical, device and biotechnology companies to improve patient care, develop new therapies and achieve scientific breakthroughs. In order to promote an ethical and transparent environment for conducting research, providing clinical care and teaching, Mount Sinai requires that salaried faculty inform the School of their relationships with such companies.
Below are financial relationships with industry reported by Dr. Krauss during 2016 and/or 2017. Please note that this information may differ from information posted on corporate sites due to timing or classification differences.
- Boehringer Ingelheim Corporation
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