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Emx1  -  empty spiracles homeobox 1

Mus musculus

Synonyms: Empty spiracles homolog 1, Empty spiracles-like protein 1, Emx-1, Homeobox protein EMX1
 
 
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High impact information on Emx1

  • Finally, Emx1 expression is exclusively confined to the dorsal telencephalon [1].
  • Mammalian homeogenes of the Emx family, Emx1 and Emx2, are expressed in the developing cerebral cortex and are involved in the patterning of the rostral brain [2].
  • Although very little is known about the role of Emx1, details of the function of EMX2 are emerging from the observation of cortical phenotypes in normal and mutant mice [2].
  • Genetic lineage tracing demonstrates that the GABA INs comprising the ectopias are from a cortical Emx1 lineage generated in the dTel VZ, definitively showing that dTel progenitors and progeny acquire a ventral, GE, fate in Pax6 mutants [3].
  • Absence of Cajal-Retzius cells and subplate neurons associated with defects of tangential cell migration from ganglionic eminence in Emx1/2 double mutant cerebral cortex [4].
 

Biological context of Emx1

  • Mapping of Vax2 between D6Mit3 and D6Mit8 on chromosome 6 indicated a possible linkage with Emx1 [5].
  • The homeobox transcription factors Emx1 and Emx2 are expressed in overlapping patterns that include cortical progenitors in the dorsal telencephalic neuroepithelium [6].
  • Thus, the PAC-Emx1#1 clone contains essentially all regulatory elements necessary for Emx1 gene expression [7].
  • In all three lines, especially Tg3, Cre-mediated recombination was highly restricted to Emx1-expressing cell lineages, from embryonic stages to adulthood [7].
 

Anatomical context of Emx1

  • Emx1, emx2 and pax6 in specification, regionalization and arealization of the cerebral cortex [8].
  • These observations indicate that the expression levels of Emx1 and/or Emx2 restrict the prospective choroid plexus territory, a novel role of these transcription factors [9].
  • In the present study we show that Emx1 and Emx2 double mutant neocortex is much more severely affected [4].
  • Emx2 most likely delineates the palliochoroidal boundary in the absence of Emx1 expression during early dorsal forebrain patterning [10].
  • Thus, the homeobox gene Emx1 can be reliably used as a marker of the pyramidal cell lineage [11].
 

Associations of Emx1 with chemical compounds

  • Double-labelling experiments confirmed that the vast majority of Emx1-expressing cells also contained glutamate, a marker of pyramidal neurons [11].
 

Other interactions of Emx1

  • On a molecular level, disruption of dorsal telencephalon development in Xt(J)/Xt(J) embryos correlates with a loss of Emx1 and Emx2 expression [12].
  • The Emx1 expression domain includes the dorsal telencephalon and it has a posterior boundary slightly anterior to that between the presumptive diencephalon and telencephalon, whereas the Otx2 expression domain covers almost the entire forebrain and midbrain [13].
  • We found that Emx2 is expressed exclusively in proliferating cells of the ventricular zone whereas Emx1 is expressed in both proliferating and differentiated neurons, throughout the cortical layers and during all the developmental stages examined [14].
  • Addition of Noggin to the culture induced prominent proliferation of the neuroepithelial cells, leading to epithelial hyperstratification of the structures. mRNAs of transcription factors essential for forebrain development such as Emx1/2 and Pax6 were specifically expressed and Islet1+Lim1/2- motoneurons appeared by the addition of Noggin [15].
  • Expression of the Emx-1 and Dlx-1 homeobox genes define three molecularly distinct domains in the telencephalon of mouse, chick, turtle and frog embryos: implications for the evolution of telencephalic subdivisions in amniotes [16].
 

Analytical, diagnostic and therapeutic context of Emx1

  • In order to better understand the role of Emx1 and Emx2 in the maturation of the cortex we analysed by in situ hybridization their expression patterns in the developing mouse cerebral cortex, from embryonic day 12.5 to adulthood [14].
  • The present study examined the phenotypes of Emx1-deficient mice generated by gene targeting technology in a battery of behavioral tests with a fixed inter-trial interval of 7 days [17].
  • Immunocytochemistry using Emx1, a marker for pyramidal neurons, indicates that the vast majority of Dab1(+/+) neurons in the supercortex were Emx1 immunoreactive [18].

References

  1. Nested expression domains of four homeobox genes in developing rostral brain. Simeone, A., Acampora, D., Gulisano, M., Stornaiuolo, A., Boncinelli, E. Nature (1992) [Pubmed]
  2. Emx homeogenes and mouse brain development. Cecchi, C., Boncinelli, E. Trends Neurosci. (2000) [Pubmed]
  3. Ventralized dorsal telencephalic progenitors in Pax6 mutant mice generate GABA interneurons of a lateral ganglionic eminence fate. Kroll, T.T., O'Leary, D.D. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  4. Absence of Cajal-Retzius cells and subplate neurons associated with defects of tangential cell migration from ganglionic eminence in Emx1/2 double mutant cerebral cortex. Shinozaki, K., Miyagi, T., Yoshida, M., Miyata, T., Ogawa, M., Aizawa, S., Suda, Y. Development (2002) [Pubmed]
  5. Expression of the Vax family homeobox genes suggests multiple roles in eye development. Ohsaki, K., Morimitsu, T., Ishida, Y., Kominami, R., Takahashi, N. Genes Cells (1999) [Pubmed]
  6. Emx1 and Emx2 cooperate to regulate cortical size, lamination, neuronal differentiation, development of cortical efferents, and thalamocortical pathfinding. Bishop, K.M., Garel, S., Nakagawa, Y., Rubenstein, J.L., O'Leary, D.D. J. Comp. Neurol. (2003) [Pubmed]
  7. Dorsal telencephalon-specific expression of Cre recombinase in PAC transgenic mice. Iwasato, T., Nomura, R., Ando, R., Ikeda, T., Tanaka, M., Itohara, S. Genesis (2004) [Pubmed]
  8. Emx1, emx2 and pax6 in specification, regionalization and arealization of the cerebral cortex. Muzio, L., Mallamaci, A. Cereb. Cortex (2003) [Pubmed]
  9. The transcription factors Emx1 and Emx2 suppress choroid plexus development and promote neuroepithelial cell fate. von Frowein, J., Wizenmann, A., Götz, M. Dev. Biol. (2006) [Pubmed]
  10. Emx1 and Emx2 functions in development of dorsal telencephalon. Yoshida, M., Suda, Y., Matsuo, I., Miyamoto, N., Takeda, N., Kuratani, S., Aizawa, S. Development (1997) [Pubmed]
  11. Emx1 is a marker for pyramidal neurons of the cerebral cortex. Chan, C.H., Godinho, L.N., Thomaidou, D., Tan, S.S., Gulisano, M., Parnavelas, J.G. Cereb. Cortex (2001) [Pubmed]
  12. Gli3 is required for Emx gene expression during dorsal telencephalon development. Theil, T., Alvarez-Bolado, G., Walter, A., Rüther, U. Development (1999) [Pubmed]
  13. Emx and Otx gene expression in the developing mouse brain. Boncinelli, E., Gulisano, M., Spada, F., Broccoli, V. Ciba Found. Symp. (1995) [Pubmed]
  14. Emx1 and Emx2 show different patterns of expression during proliferation and differentiation of the developing cerebral cortex in the mouse. Gulisano, M., Broccoli, V., Pardini, C., Boncinelli, E. Eur. J. Neurosci. (1996) [Pubmed]
  15. Noggin and basic FGF were implicated in forebrain fate and caudal fate, respectively, of the neural tube-like structures emerging in mouse ES cell culture. Chiba, S., Kurokawa, M.S., Yoshikawa, H., Ikeda, R., Takeno, M., Tadokoro, M., Sekino, H., Hashimoto, T., Suzuki, N. Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. (2005) [Pubmed]
  16. Expression of the Emx-1 and Dlx-1 homeobox genes define three molecularly distinct domains in the telencephalon of mouse, chick, turtle and frog embryos: implications for the evolution of telencephalic subdivisions in amniotes. Fernandez, A.S., Pieau, C., Repérant, J., Boncinelli, E., Wassef, M. Development (1998) [Pubmed]
  17. Reduced anxiety-- and depression-like behaviors in Emx1 homozygous mutant mice. Cao, B.J., Li, Y. Brain Res. (2002) [Pubmed]
  18. disabled-1 functions cell autonomously during radial migration and cortical layering of pyramidal neurons. Hammond, V., Howell, B., Godinho, L., Tan, S.S. J. Neurosci. (2001) [Pubmed]
 
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