Neuron‐specific enolase‐cre mouse line with cre activity in specific neuronal populations

To establish genetic tools for conditional gene deletion in mouse neurons, we generated two independent neuron‐specific enolase (Nse)‐cre transgenic lines. The transgenic line termed Nse‐creCK1 showed cre activity in most neuronal regions in the nervous system, while the Nse‐creCK2 line exhibited a unique cre activity that has not been reported in other cre transgenic lines. Nse‐creCK2 cre activity was detectable from embryogenesis and mostly restricted to neuronal regions. In postnatal brain, the Nse‐creCK2 line exhibited cre activity limited to differentiated neurons in the cerebral cortex and hippocampus. Cre activity was assayed in several internal organs and sporadic activity was limited to the kidney and testis. We conclude that these cre lines will be useful for studying loss of gene function in specific neuronal populations. genesis 44:130–135, 2006. Published 2006 Wiley‐Liss, Inc.

[1]  Yun-Fai Chris Lau,et al.  A Cre gene directed by a human TSPY promoter is specific for germ cells and neurons , 2005, Genesis.

[2]  B. Luikart,et al.  TrkB Has a Cell-Autonomous Role in the Establishment of Hippocampal Schaffer Collateral Synapses , 2005, The Journal of Neuroscience.

[3]  D. Gutmann,et al.  Pten Loss Causes Hypertrophy and Increased Proliferation of Astrocytes In vivo , 2004, Cancer Research.

[4]  C. Stiles,et al.  Molecular mechanisms controlling cortical gliogenesis , 2002, Current Opinion in Neurobiology.

[5]  F. Sablitzky,et al.  Cre‐mediated transgene activation in the developing and adult mouse brain , 2001, Genesis.

[6]  L. Gudas,et al.  cis-acting DNA regulatory elements, including the retinoic acid response element, are required for tissue specific laminin B1 promoter/lacZ expression in transgenic mice , 2001, Mechanisms of Development.

[7]  Caiying Guo,et al.  Z/EG, a double reporter mouse line that expresses enhanced green fluorescent protein upon cre‐mediated excision , 2000, Genesis.

[8]  C. Sigmund.  Viewpoint: are studies in genetically altered mice out of control? , 2000, Arteriosclerosis, thrombosis, and vascular biology.

[9]  T. Palmer,et al.  Neurogenesis in the dentate gyrus of the adult rat: age-related decrease of neuronal progenitor proliferation , 1996, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[10]  L. Tessarollo,et al.  Targeted mutation in the neurotrophin-3 gene results in loss of muscle sensory neurons. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[11]  K. Rajewsky,et al.  Independent control of immunoglobulin switch recombination at individual switch regions evidenced through Cre-loxP-mediated gene targeting , 1993, Cell.

[12]  M. Nerenberg,et al.  Transgenic mice expressing β-galactosidase in mature neurons under neuron-specific enolase promoter control , 1990, Neuron.

[13]  R. Hoess,et al.  Interaction of the bacteriophage P1 recombinase Cre with the recombining site loxP. , 1984, Proceedings of the National Academy of Sciences of the United States of America.

[14]  J. Strathern,et al.  Genetics of Lactase Persistence and Lactose Intolerance , 2008 .

[15]  Philippe Soriano.  Generalized lacZ expression with the ROSA26 Cre reporter strain , 1999, Nature Genetics.

[16]  M. C. Whitehead,et al.  Synapse formation is related to the onset of neuron-specific enolase immunoreactivity in the avian auditory and vestibular systems. , 1982, Developmental neuroscience.