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everal distinct cell types in the adult central nervous
0 S& f6 E1 l/ G! n( hsystem have been suggested to act as stem or prog-
. s0 [/ t+ F/ G# R( \8 g" Henitor cells generating new cells under physiological6 X) j7 H0 m/ }; [$ l( N
or pathological conditions. We have assessed the3 O6 W7 n* g8 h& } e% V$ u$ w
origin of new cells in the adult mouse spinal cord by
1 I3 [* q5 d. f9 q }4 w/ t2 ?genetic fate mapping. Oligodendrocyte progenitors5 x1 s2 Q# f6 ]' b2 T# Z& E' Y
self-renew, give rise to newmature oligodendrocytes,
. V5 R. ~) v/ ~4 qand constitute the dominating proliferating cell popu-
5 p' r' G8 z2 e1 B! n* Y: l9 A; [lation in the intact adult spinal cord. In contrast, astro-+ ]6 n) @# E$ U
cytes and ependymal cells, which are restricted to& |+ ?" n9 j& _+ M
limited self-duplication in the intact spinal cord,) V7 V" J9 \7 F: {2 c+ M0 V. ?5 B
generate the largest number of cells after spinal cord
/ [$ \9 g- U$ |$ Minjury. Only ependymal cells generate progeny of! @4 b1 Y+ n' C) B8 j/ y+ U v
multiple fates, and neural stemcell activity in the intact' X, J9 O/ i+ g
and injured adult spinal cord is confined to this cell
) P% N7 G7 R/ t- J: V0 B. P- q. rpopulation. We provide an integrated view of how$ ^0 r# g+ f; ~; J& M
severaldistinct cell types contribute in complementary
+ @7 u- n9 I& B) N5 ?/ ]! h2 g# Sways to cell maintenance and the reaction to injury. |
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