Faculty Profile

Dr. Jean M. Hebert, Ph.D.

Jean M. Hebert, Ph.D.

Professor, Dominick P. Purpura Department of Neuroscience

Professor, Department of Genetics

Areas of Research: Understanding how embryonic neural precursors generate the neocortex, the seat of our highest cognitive functions, and devising methods of regenerating the principle neurons of the adult neocortex when they are lost.

Professional Interests

Regenerating the neocortex

 

The Hébert lab has two general areas of interest. First, the lab is studying how homeostasis is maintained in the adult cerebral cortex, which includes the hippocampus and neocortex, the part of our brains that we use for our highest cognitive and perceptual functions. Specifically, the lab examines how neurogenesis is sustained in the hippocampus and how the myelination of axons is maintained through continuous oligodendrogenesis. The lab uses primarily molecular genetic techniques to manipulate the expression of regulatory genes in neural stem and progenitor cells. Second, the lab is developing novel methods to repair the neocortex upon loss of neurons. Neocortical damage can be local, due for example to stroke or trauma, or widespread, due to neurodegeneration or aging. Hence we are developing ways of either locally or broadly replacing the principle neurons of the adult neocortex without significantly disrupting the function of existing neural circuits. These approaches involve transplanting mixed precursor cell populations as well as engineering precursor cells that can disperse widely throughout the neocortex to repopulate existing circuits with new cells and bolster the function of these circuits.

 

Selected Publications

Selected Publications

Nandi S, Gutin G, Blackwood CA, Kamatkar NG, Lee KW, Fishell G, Wang F, Goldfarb M, Hébert JM. (2017). Context-driven, receptor-dependent usage of an intracellular adapter governs specificity in FGF signal transduction. J. Neurosci. 37:5690-5698.

Antoine MW, Vijayakumar S, McKeehan N, Jones S, Hébert, JM. (2017). The severity of vestibular dysfunction in deafness as a determinant of comorbid hyperactivity or anxiety. J. Neurosci. 37: 5144-5154.

Andriani GA, Faggioli F, Baker D, Dollé MET, Sellers RS, Hébert JM, van Steeg H, Hoeijmakers J, Vijg J, Montagna C. (2016). Whole chromosome aneuploidy in the brain of BubR1H/H  and Ercc1 -/Δ7 mice. Hum. Mol. Gen. 25: 755-765.

Nandi S, Chandramohan D, Fioriti L, Melnick AM, Hébert JM, Mason CE, Kandel ER, Rajasethupathy P. (2016). A role for piRNAs in retrotransposon silencing in the mammalian brain. P.N.A.S. U.S.A. 113: 12696-12702.

Kang W, Hébert JM. (2015). FGF signaling is necessary for neurogenesis in young mice and sufficient to reverse its decline in old mice. J. Neuroscience 35: 10217-10223.

Kang W, Balordi F, Su N, Chen L, Fishell G, Hébert JM. (2014). Astrocyte activation in both normal and injured brain is suppressed by FGF signaling. PNAS, 111: E2987-E2995.

Antoine M, Hübner CA, Arezzo JC, Hébert JM. (2013). A causative link between inner ear defects and long-term striatal dysfunction. Science 341: 1120-1123.

Diaz F, McKeehan N, Kang W, Hébert JM. (2013). Apoptosis of glutamatergic neurons fails to trigger a neurogenic response in the adult neocortex. J. Neuroscience 33: 6278-6284.

Hébert JM. (2013). Only scratching the cell surface; extracellular signals in cerebrum development. Curr. Opin. Genet. Dev. 23: 470-474.

Tole S, Hébert JM. (2013). Telencephalic patterning. In “Patterning and cell type specification in the developing CNS and PNS, Comprehensive Developmental Neuroscience”, Volume 1, Elsevier, ed. Pasko Rakic and John Rubenstein. p. 3-24.

Paek H, Antoine M, Diaz F, Hébert JM. (2012). Increased -catenin activity in the anterior neural plate induces ectopic mid-hindbrain characteristics. Dev. Dyn. 241: 242-246.

Fernandes M, Antoine M, Hébert JM. (2012). SMAD4 is essential in generating rhombic lip-derived neurons during cerebellar development. Dev. Biol. 365: 82-90.

Kang W, Hébert JM. (2012). A Sox2 BAC transgenic approach for targeting adult neural stem cells. PLoS ONE 7: e49038.

Khonsari RH, Delezoide AL, Kang W, Hébert JM, Bessières B, Bodiguel V, Collet C, Legeai-Mallet L, Sharpe PT, Fallet-Bianco C. (2012). Central nervous system malformations and deformations in FGFR2-related craniosynostosis. Am. J. Med. Genet. PartA 158: 2797-2806. PMID 22987770.

Paek H, Hwang JY, Zukin RS, Hébert JM. (2011). b-catenin-dependent FGF signaling sustains cell survival in the anterior embryonic head by countering Smad4Developmental Cell 20: 689-699.

Hébert JM. (2011). FGFs: neurodevelopment's Jack-of-all-trades - how do they do it? Frontiers in Neurogenesis 5: 133.

Kang W, Hébert JM. (2011).  Signaling pathways in reactive astrocytes, a genetic perspective. Mol. Neurobiol. 43: 147-154.

Furusho M, Kaga Y, Ishii A, Hébert JM, Bansal R. (2011). FGF signaling is required for the generation of oligodendrocyte progenitors from the embryonic forebrain. J. Neurosci. 31: 5055-5066.

Ferretti E, Li B, Zewdu R, Wells V, Hébert JM, Karner C, Anderson MJ, Williams T, Dixon J, Dixon MJ, Depew MJ, Selleri L. (2011). A Conserved Pbx-Wnt-p63-Irf6 Regulatory Module Controls Face Morphogenesis by Promoting Epithelial Apoptosis. Dev. Cell 21: 627-641.

Maier E, von Hofsten J, Nord H, Fernandes M, Paek H, Hébert JM, Gunhaga L. (2010). Opposing activities of FGF and BMP regulate the olfactory sensory versus respiratory epithelial cell fate decision. Development 137: 1601-1611.

Paek H, Gutin G, Hébert JM. (2009). FGF signaling is strictly required to maintain early telencephalic precursor cell survival. Development 136: 2457-2465.

Kang W, Wong LC, Shi S, Hébert JM. (2009). The transition from radial glial to intermediate progenitor cell is inhibited by FGF signaling during corticogenesis. J. Neurosci. 29: 14571-14580.

Hébert JM, Fishell G. (2008). The genetics of telencephalon patterning, some assembly required. Nat. Rev. Neurosci., 9: 678-685.

Chang W, Lin Z, Kulessa H, Hébert J, Hogan BLM, Wu DK. (2008). Bmp4 is essential for the formation of the vestibular apparatus that detects angular head movements. PLoS Genetics 4: e1000050. PMID: 18404215, PMCID: PMC2274953.

Zhou L, Bar I, Achouri Y, Campbell K, De Backer O, Hébert JM, Jones K, Kessaris N, de Rouvroit CL, Richardson WD, O’Leary D, Goffinet AM, Tissir F. (2008). Early forebrain wiring: genetic dissection using conditional Celsr3 mutant mice. Science 320: 946-949. PMID: 18487195, PMCID: PMC2746700.

Fernandes M, Hébert JM. (2008). The ups and downs of holoprosencephaly, dorsal versus ventral patterning forces. Clin. Gen. 73: 413-423.

Fernandes M, Gutin G, Alcorn H, McConnell SK, Hébert JM. (2007). Mutations in the BMP pathway in mice supports the existence of two molecular classes of holoprosencephaly. Development 134: 3789-3794. PMID: 17913790.

Hanashima C, Fernandes M, Hébert JM, Fishell G. (2007). The role of Foxg1 and dorsal midline signaling in the generation of Cajal-Retzius subtypes. J. Neurosc. 27: 11103-11111. PMID: 17928452.

Gutin G*, Fernandes M*, Pallazolo L, Paek H, Kai Y, Ornitz D, McConnell SK, Hébert JM. (2006). FGF acts independently of SHH to generate ventral telencephalic cells. Development 133: 2937-2946. PMID: 16818446.   *co-first authors

Arnold JS, Werling U, Braunstein EM, Liao J, Nowotschin S, Edelmann W, Hébert JM, Morrow BE. (2006). Inactivation of Tbx1 in the pharyngeal endoderm results in 22q11DS malformations. Development 133: 977-987.

Tole S*, Gutin G*, Remedios R, Bhatnagar L, Hébert JM. (2006). Development of midline cell types and commissural axon tracts requires Fgfr1 in the cerebrum. Dev. Biol. 289: 141-151. PMID: 16309667.  *co-first authors

Hébert JM. (2005). Unraveling the molecular pathways that regulate early telencephalon development. Curr. Top. in Dev. Biol. 69: 17-37.

 

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More Information About Dr. Jean Hebert

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Albert Einstein College of Medicine
Rose F. Kennedy Center
1410 Pelham Parkway South , Room 237
Bronx, NY 10461

Tel: 718.430.3494

Research Information

In the News

The New York Times interviews Dr. Jean Hébert about his research featured in Science that found a link between hyperactivity and an inner ear defect in mice.

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