Novel genetic tools facilitate the study of cortical neuron migration

Abstract

Key facets of mammalian forebrain cortical development include the radial migration of projection neurons and subsequent cellular differentiation into layer-specific subtypes. Inappropriate regulation of these processes can lead to a number of congenital brain defects in both mouse and human, including lissencephaly and intellectual disability. The genes regulating these processes are still not all identified, suggesting genetic analyses will continue to be a powerful tool in mechanistically studying the development of the cerebral cortex. Reelin is a molecule which we have understood to be critical for proper cortical development for many years. The precise mechanism of Reelin, however, is not fully understood. To address both of these unresolved issues, we report here the creation of a novel conditional allele of the Reelin gene and showcase the use of an Etv1-GFP transgenic line highlighting a subpopulation of the cortex: layer V pyramidal neurons. Together, these represent genetic tools which may facilitate the study of cortical development in a number of different ways.

Nubp2is required for cranial neural crest survival in the mouse

“…Wildtype C57BL/6J (B6; Jackson Laboratory, Bar Harbor ME) 6-to 8-week-old males were given a fractionated dose of ENU (three weekly dosages of 90-100 mg/kg ENU, Sigma). Mutagenized males were bred with Tg(Etv1-EGFP) B2192 GSat females (FVB/N TaC background) as part of a larger effort to identify potential mutants in cortical neuron patterning [28]. Following a three-generation backcross breeding scheme [18], G3 litters were dissected at late embryonic stages to detect gross developmental anomalies.…”

Nubp2 is required for cranial neural crest survival in the mouse

“…Harbor ME) 6-to 8-week-old males were given a fractionated dose of ENU (three weekly dosages of 90-100 mg/kg ENU, Sigma). Mutagenized males were bred with Tg(Etv1-EGFP) B2192 GSat females (FVB/N TaC background) as part of a larger effort to identify potential mutants in cortical neuron patterning [28]. Following a three-generation backcross breeding scheme [18], G3 litters were dissected at late embryonic stages to detect gross developmental anomalies.…”