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Gene: GMCL1L  -  germ cell-less homolog 1 (Drosophila)-like

Homo sapiens

Synonyms: GCL, Germ cell-less protein-like 1-like, GMCL2
 
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Disease relevance of GMCL1L

  • A model system for studying these programs is the ganglion cell layer (GCL) of the vertebrate retina because of its simple and well-described structure and amenability to experimental manipulations [1].
  • PURPOSE: Pathophysiological events in the retinal ganglion cell layer (GCL) are a prominent feature of several optic neuropathies including glaucoma [2].
 

High impact information on GMCL1L

  • The GCL contains approximately equal numbers of ganglion cells and displaced amacrine cells [1].
  • Roughly half of GCL neurons die during development in amniotes, whereas developmental cell death does not occur in the GCL neurons of anamniotes [1].
  • Stimulation of the lateral olfactory tract (LOT) produced a negative field potential in the EPL and a positivity in the GCL [3].
  • Dendrodendritic synapses from mitral/tufted cells occur on granule cell distal dendrites in the external plexiform layer (EPL), whereas CFFs preferentially target the somata/proximal dendrites of granule cells in the granule cell layer (GCL) [3].
  • Adult subgranular zone cells migrated into the DG granule cell layer (GCL), assumed a neuronal phenotype and demonstrated seizure-dependent responsiveness [4].
 

Biological context of GMCL1L

  • Neurogenesis and cell death have been studied extensively in the GCL of various amniotes (rodents, chicks, and monkeys) and anamniotes (fish and frogs), and the two processes highlight developmental differences between the groups [1].
  • CONCLUSIONS: We have successfully used LCM technology to generate gene expression profiles of highly enriched GCL fractions of the normal human retina [2].
  • Using bioinformatics approaches over 80 genes were identified whose expression in the human retina appears to be limited to the GCL [2].
  • In contrast, transcripts for genes associated with phototransduction (RHO), photoreceptor development (NR2E3), or interphotoreceptor matrix constituents (IMPG1) were nearly absent from the GCL fraction [2].
 

Anatomical context of GMCL1L

  • The ischemia-induced changes in trkA immunoreactivity were found in the polymorphic layer (PL) and granule cell layer (GCL) of the dentate gyrus [5].
  • Thus, Olig2 is an marker both for retinal progenitor cells during embryonic stages, and also for differentiated retinal subpopulations within the GCL and INL during postnatal stages [6].
 

Associations of GMCL1L with chemical compounds

  • In sham-operated rats, the numbers of BrdU-labeled cells were significantly increased (2.2-fold) in the SGZ and GCL in response to running exercise [7].

References

  1. Neurogenesis and cell death in the ganglion cell layer of vertebrate retina. Farah, M.H. Brain Res. Brain Res. Rev. (2006)
  2. Gene expression profile of the adult human retinal ganglion cell layer. Kim, C.Y., Kuehn, M.H., Clark, A.F., Kwon, Y.H. Mol. Vis. (2006)
  3. Complementary postsynaptic activity patterns elicited in olfactory bulb by stimulation of mitral/tufted and centrifugal fiber inputs to granule cells. Laaris, N., Puche, A., Ennis, M. J. Neurophysiol. (2007)
  4. Functional dentate gyrus neurogenesis in a rapid kindling seizure model. Smith, P.D., McLean, K.J., Murphy, M.A., Turnley, A.M., Cook, M.J. Eur. J. Neurosci. (2006)
  5. Transient ischemia-induced expression and changes of tyrosine kinase A in the hippocampal dentate gyrus of the gerbil. Hwang, I.K., Lee, H.Y., Yoo, K.Y., Kim, D.H., Kim, J.H., Kim, C.H., Lim, B.O., Kang, T.C., Bang, K.H., Seong, N.S., Lee, H.J., Kim, J.D., Won, M.H. Int. J. Neurosci. (2006)
  6. Expression of the basic helix-loop-factor Olig2 in the developing retina: Olig2 as a new marker for retinal progenitors and late-born cells. Shibasaki, K., Takebayashi, H., Ikenaka, K., Feng, L., Gan, L. Gene Expr. Patterns (2007)
  7. Postischemic exercise decreases neurogenesis in the adult rat dentate gyrus. Yagita, Y., Kitagawa, K., Sasaki, T., Terasaki, Y., Todo, K., Omura-Matsuoka, E., Matsumoto, M., Hori, M. Neurosci. Lett. (2006)
 
 
 
 
 
 
 
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