PMID- 10545161
OWN - NLM
STAT- MEDLINE
DCOM- 19991210
LR  - 20190905
IS  - 0021-9967 (Print)
IS  - 0021-9967 (Linking)
VI  - 415
IP  - 2
DP  - 1999 Dec 13
TI  - Callosal axon guidance defects in p35(-/-) mice.
PG  - 218-29
AB  - Mice lacking p35, an activator of cdk5 in the central nervous system (CNS),
      exhibit defects in a variety of CNS structures, most prominently characterized by
      a disruption in the laminar structure of the neocortex (Chae et al., 1997). In
      addition, alterations of certain axonal fiber tracts are found in the cortex of
      p35 mutant mice. Notably, the corpus callosum appears bundled at the midline, but
      dispersed lateral to the midline. Tracer injection experiments in adult p35
      mutant mice reveal that projecting cortical axons fail to assimilate into the
      corpus callosum, and take oblique paths to the midline. After crossing the
      midline, cortical axons defasciculate prematurely from the corpus callosum and
      take similarly oblique paths through the cortex. This callosal phenotype is not
      detected in reeler mice, which also exhibit defects in cortical lamination,
      suggesting that the lack of fasciculation of callosal axons is not an inherent
      manifestation of a disruption of cortical lamination. The embryonic callosal axon
      tract is defasciculated before crossing the midline, suggesting that axon
      guidance may be affected during embryonic development of the corpus callosum. In 
      addition, embryonic thalamocortical afferents also exhibit a defasciculated
      phenotype. These results suggest that defective axonal fasciculation and guidance
      may be primary responses to the loss of p35 in the cortex. Furthermore, this
      study postulates a role for the p35/cdk5 kinase in molecular signaling pathways
      necessary for proper guidance of selective axons during embryonic development.
CI  - Copyright 1999 Wiley-Liss, Inc.
FAU - Kwon, Y T
AU  - Kwon YT
AD  - Howard Hughes Medical Institute, Department of Pathology, Harvard Medical School,
      Boston, Massachusetts 02115, USA.
FAU - Tsai, L H
AU  - Tsai LH
FAU - Crandall, J E
AU  - Crandall JE
LA  - eng
GR  - GM53049/GM/NIGMS NIH HHS/United States
GR  - NS24386/NS/NINDS NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Comp Neurol
JT  - The Journal of comparative neurology
JID - 0406041
RN  - 0 (3,3'-dihexadecylindocarbocyanine)
RN  - 0 (Bacterial Outer Membrane Proteins)
RN  - 0 (Carbocyanines)
RN  - 0 (Cdk5r1 protein, mouse)
RN  - 0 (Lipoproteins)
RN  - EC 2.7.- (Phosphotransferases)
RN  - EC 2.7.11.1 (Cyclin-Dependent Kinase 5)
RN  - EC 2.7.11.22 (Cdk5 protein, mouse)
RN  - EC 2.7.11.22 (Cyclin-Dependent Kinases)
SB  - IM
MH  - *Agenesis of Corpus Callosum
MH  - Animals
MH  - Axons/*physiology/ultrastructure
MH  - Bacterial Outer Membrane Proteins/*genetics
MH  - Carbocyanines
MH  - Corpus Callosum/*cytology
MH  - Cyclin-Dependent Kinase 5
MH  - Cyclin-Dependent Kinases/physiology
MH  - Immunohistochemistry
MH  - Lipoproteins/*genetics
MH  - Mice
MH  - Mice, Knockout/*abnormalities
MH  - Mice, Mutant Strains/abnormalities
MH  - Mice, Neurologic Mutants/abnormalities
MH  - Neural Pathways/abnormalities/cytology
MH  - *Phosphotransferases
MH  - Somatosensory Cortex/abnormalities/cytology
MH  - Thalamus/abnormalities/cytology
EDAT- 1999/11/02 00:00
MHDA- 1999/11/02 00:01
CRDT- 1999/11/02 00:00
PHST- 1999/11/02 00:00 [pubmed]
PHST- 1999/11/02 00:01 [medline]
PHST- 1999/11/02 00:00 [entrez]
AID - 10.1002/(SICI)1096-9861(19991213)415:2<218::AID-CNE6>3.0.CO;2-F [pii]
AID - 10.1002/(sici)1096-9861(19991213)415:2<218::aid-cne6>3.0.co;2-f [doi]
PST - ppublish
SO  - J Comp Neurol. 1999 Dec 13;415(2):218-29. doi:
      10.1002/(sici)1096-9861(19991213)415:2<218::aid-cne6>3.0.co;2-f.