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LIFR stimulates the proliferation of neural stem cell
638
THE ACTIVATION
TAKATOSHI
UEKII,:,
OF gpl3O/LIFR
STIMULATES
TOSHlO HEIKE?, TAKASHI
THE PROLIFERATION
OF NEURAL STEM CELL.
YOKOTA’.
adept. of Biorcgulation Rcs., Nagoya City Univ. Med. Sch., Mizuho-ku, Nagoya 467-0001, Regulation, Inst. of Med. Sci., Univ. of Tokyo, Minato-ku. Tokyo 108-8639.
ZDept. of Stem Cell
The self-rcncwal mechanism of mammmalian brain neural stem cell has well been studied until recently, and one of them is Ras-MAPK signal pathway activated by EGF and bFGF. But littlc is known about the role of JAK-Tyk family signal oathwav in neural stem cell. In this studv the influence of LIFR/eo130 activation on neural stem cell oroliferation was Examined. From the transgcnic mouse embryo expressing huma;;‘GM-CSFR extracellular domain aid LIFR/gpl30 intracellular domain. striatal neural stem cell was prepared. After that human GM-CSF was added and the effect on neural stem cell was ana,lyzcd. It was shown that human GM-CSF promoted the proliferation of neural stem cell with doscdcpcndcncy, but its mitogenic activity was wcakcr than that of mouse EGF. And neural stem cell differentiated into neuron, astrocytc and oligodcndrocytc without human GM-CSF. In this study, the conclusion was that the JAK-Tyk family signal pathway via LIFRigpl30 was involved in brain neural stem cell self-renewal mechanism. The existcncc of another signal pathway involved in neural stem ccl1 proliferation implies its different role in nerve injury or regeneration.
639
VISUALIZATION
MASAHIRO
YAMAGUCHII.2,
OF NELJRONAL STEM CELLS IN VIVO
MISAO SUZUKI-‘, KENSAKU
MORI2
‘PRESTO, Japan Science md Technology Corporation, Soraku-gun, Kyoto 61 Y-0237, 2Lab. for Neuronal Recognition Molecules, Bran Science Institute, RIKEN. Wake, Saitama 35 I-0198. iCenter for Animal Resources and Development, Kumnmoto Univ., Kuhonji, Kumamoto X62-0976
Neuronal stem cells (NSC) having self-renewal
capacity and multi-potency
play an essential role in brain development.
NSC
exist also in adult mammalian
brain. Thus, studying the distribution and fate of NSC in vivo would lead to the understanding
of the process of organization
and plastic changes of the neuronal circuit during development
the generation
of transgenic
mice in which NSC can be easily visualized by introducing green fluorescent
cDNA under the control of the nestin promoter, which drives NSC-specific mice, GFPfluorescence
expression.
was observed in several regions including subependymal
olfactory bulb, where existence
MOUSE
MUSASHI-1,
IN MAMMALIAN
SHIN-ICHI SAKAKIBARAI,2,
protein (GFP)
In the adult brain of the transgenic
zone, dentate gyrus of hippocampus,
and
of NSC has been suggested. These mice would be a useful tool to reveal the dynamic
behavior of the NSC in the brain as well as their contribution
640
and in adults. Here we report
to the plasticity of the neuronal circuit.
A RNA-BINDING NEURAL
PROTEIN
PRECURSOR
YUKI NAKAMURAI,
ENRICHED
CELLS.
HIROSHI TAKAN03. TETSUO NODA3, and HIDEYUKI 0KAN01.2
I Dept. of Neuroanatomy, Osaka Univ. Medical School. Suita, Osaka 565. 2CREST, Japan Sci. and Tech. Corp. (JST), Shinagawa-ku, Tokyo 140. 3Department of CeII Biology, Cancer Institute, Toshima-kwu, Tokyo 170 mouse Musashi-1
(m-Msi-1)
are capable of generating the proliferative subventricular
neuronal
in the external
protein which is associated CNS development.
the persistent
glial precursors
remained in the proliferating
(neural stem cells).
To elucidate
cells that
m-Msi-1 was expressed
in
and in the anterior comer of the
expression
of m-Msi-1 was observed
in SVZ to the differentiated
astrocytes
in
in the
cells in adult SVZ which is recently suggested
the function
a targeted disruption of the m-msi-1 locus. The phenotype
with neural precursor
Postnatally,
granule cell layer of cerebellum,
During gliogenesis,
lineage ranging from the proliferative
In addition, m-Msi-1 expression
to contain neural precursors performed
precursors
zone (SVZ) of lateral ventricles.
cells of the astrocyte parenchyma.
is a mouse neural RNA-binding
neurons and glia during embryonic
of m-Msi-1
of homozygous
during CNS development,
mutant mice is currently examined.
we
THE ACTIVATION
TAKATOSHI
UEKII,:,
OF gpl3O/LIFR
STIMULATES
TOSHlO HEIKE?, TAKASHI
THE PROLIFERATION
OF NEURAL STEM CELL.
YOKOTA’.
adept. of Biorcgulation Rcs., Nagoya City Univ. Med. Sch., Mizuho-ku, Nagoya 467-0001, Regulation, Inst. of Med. Sci., Univ. of Tokyo, Minato-ku. Tokyo 108-8639.
ZDept. of Stem Cell
The self-rcncwal mechanism of mammmalian brain neural stem cell has well been studied until recently, and one of them is Ras-MAPK signal pathway activated by EGF and bFGF. But littlc is known about the role of JAK-Tyk family signal oathwav in neural stem cell. In this studv the influence of LIFR/eo130 activation on neural stem cell oroliferation was Examined. From the transgcnic mouse embryo expressing huma;;‘GM-CSFR extracellular domain aid LIFR/gpl30 intracellular domain. striatal neural stem cell was prepared. After that human GM-CSF was added and the effect on neural stem cell was ana,lyzcd. It was shown that human GM-CSF promoted the proliferation of neural stem cell with doscdcpcndcncy, but its mitogenic activity was wcakcr than that of mouse EGF. And neural stem cell differentiated into neuron, astrocytc and oligodcndrocytc without human GM-CSF. In this study, the conclusion was that the JAK-Tyk family signal pathway via LIFRigpl30 was involved in brain neural stem cell self-renewal mechanism. The existcncc of another signal pathway involved in neural stem ccl1 proliferation implies its different role in nerve injury or regeneration.
639
VISUALIZATION
MASAHIRO
YAMAGUCHII.2,
OF NELJRONAL STEM CELLS IN VIVO
MISAO SUZUKI-‘, KENSAKU
MORI2
‘PRESTO, Japan Science md Technology Corporation, Soraku-gun, Kyoto 61 Y-0237, 2Lab. for Neuronal Recognition Molecules, Bran Science Institute, RIKEN. Wake, Saitama 35 I-0198. iCenter for Animal Resources and Development, Kumnmoto Univ., Kuhonji, Kumamoto X62-0976
Neuronal stem cells (NSC) having self-renewal
capacity and multi-potency
play an essential role in brain development.
NSC
exist also in adult mammalian
brain. Thus, studying the distribution and fate of NSC in vivo would lead to the understanding
of the process of organization
and plastic changes of the neuronal circuit during development
the generation
of transgenic
mice in which NSC can be easily visualized by introducing green fluorescent
cDNA under the control of the nestin promoter, which drives NSC-specific mice, GFPfluorescence
expression.
was observed in several regions including subependymal
olfactory bulb, where existence
MOUSE
MUSASHI-1,
IN MAMMALIAN
SHIN-ICHI SAKAKIBARAI,2,
protein (GFP)
In the adult brain of the transgenic
zone, dentate gyrus of hippocampus,
and
of NSC has been suggested. These mice would be a useful tool to reveal the dynamic
behavior of the NSC in the brain as well as their contribution
640
and in adults. Here we report
to the plasticity of the neuronal circuit.
A RNA-BINDING NEURAL
PROTEIN
PRECURSOR
YUKI NAKAMURAI,
ENRICHED
CELLS.
HIROSHI TAKAN03. TETSUO NODA3, and HIDEYUKI 0KAN01.2
I Dept. of Neuroanatomy, Osaka Univ. Medical School. Suita, Osaka 565. 2CREST, Japan Sci. and Tech. Corp. (JST), Shinagawa-ku, Tokyo 140. 3Department of CeII Biology, Cancer Institute, Toshima-kwu, Tokyo 170 mouse Musashi-1
(m-Msi-1)
are capable of generating the proliferative subventricular
neuronal
in the external
protein which is associated CNS development.
the persistent
glial precursors
remained in the proliferating
(neural stem cells).
To elucidate
cells that
m-Msi-1 was expressed
in
and in the anterior comer of the
expression
of m-Msi-1 was observed
in SVZ to the differentiated
astrocytes
in
in the
cells in adult SVZ which is recently suggested
the function
a targeted disruption of the m-msi-1 locus. The phenotype
with neural precursor
Postnatally,
granule cell layer of cerebellum,
During gliogenesis,
lineage ranging from the proliferative
In addition, m-Msi-1 expression
to contain neural precursors performed
precursors
zone (SVZ) of lateral ventricles.
cells of the astrocyte parenchyma.
is a mouse neural RNA-binding
neurons and glia during embryonic
of m-Msi-1
of homozygous
during CNS development,
mutant mice is currently examined.
we