Expression pattern of aKrox-20/Cre knock-in allele in the developing hindbrain, bones, and peripheral nervous system

Voiculescu, Octavian; Charnay, Patrick; Schneider‐Maunoury, Sylvie

doi:10.1002/(sici)1526-968x(200002)26:2<123::aid-gene7>3.0.co;2-o

Cited by 156 publications

(188 citation statements)

References 8 publications

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“…To determine whether Cre-mediated recombination in the NF1flox allele results in a null allele, we crossed NF1flox/flox mice with a transgenic strain that expresses Cre recombinase in the mouse germ line (Voiculescu et al 2000). The resultant progeny harbor a recombined allele (NF1⌬) and a wild-type allele, NF1⌬/+.…”

Section: Generation Of Nf1 Conditional Mutant Mice By Cre/loxpmentioning

confidence: 81%

Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain

Zhu¹,

Romero²,

Ghosh³

et al. 2001

Genes Dev.

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551

557

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Neurofibromatosis type 1 (NF1) is a prevalent genetic disorder that affects growth properties of neural-crest-derived cell populations. In addition, approximately one-half of NF1 patients exhibit learning disabilities. To characterize NF1 function both in vitro and in vivo, we circumvent the embryonic lethality of NF1 null mouse embryos by generating a conditional mutation in the NF1 gene using Cre/loxP technology. Introduction of a Synapsin I promoter driven Cre transgenic mouse strain into the conditional NF1 background has ablated NF1 function in most differentiated neuronal populations. These mice have abnormal development of the cerebral cortex, which suggests that NF1 has an indispensable role in this aspect of CNS development. Furthermore, although they are tumor free, these mice display extensive astrogliosis in the absence of conspicuous neurodegeneration or microgliosis. These results indicate that NF1-deficient neurons are capable of inducing reactive astrogliosis via a non-cell autonomous mechanism.

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Section: Generation Of Nf1 Conditional Mutant Mice By Cre/loxpmentioning

confidence: 81%

Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain

Zhu¹,

Romero²,

Ghosh³

et al. 2001

Genes Dev.

Self Cite

551

557

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“…In this scenario, r4 neural crest are programmed, through the activity of hoxb1, to specifically interact with outgrowing motor axons of the facial nerve to provide support, guidance, or target coordinates for proper neuronal development. A nonautonomous role for hoxb1 may also rationalize the incomplete penetrance associated with the hoxb1 null mutant, a conceivable notion if glial cells derived from other rhombomeres are able to partially compensate for r4 neural crest function (Couly et al, 1996;Voiculescu et al, 2000Voiculescu et al, , 2001. This is a testable hypothesis and is currently being pursued using genetic models.…”

Section: Discussionmentioning

confidence: 99%

Hoxb1 neural crest preferentially form glia of the PNS

Arenkiel

Gaufo

Capecchi

2003

Developmental Dynamics

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The vertebrate cranial neural crest cells give rise to many complex derivatives of the head, neck, and face, including neuronal and glial cells that act in concert for proper development of the anterior-peripheral nervous system. Several genes have been implicated in the processes of neural crest specification, migration, and differentiation; among these are the hox gene clusters. To determine the fates of hox-expressing cranial neural crest, we describe the results of a genetic lineage analysis by using the Cre/loxP system to drive the activation of different ROSA26 reporter alleles under the regulation of the hoxb1 locus. By targeting the 3 untranslated region of the hoxb1 gene, we have preserved endogenous gene activity and have been able to accurately follow the fates of the cells derived from the hoxb1 expression domain. Emphasis was placed on identifying the cell and tissue types that arise from the rhombomere 4-derived neural crest. Our results demonstrate that, in addition to forming much of the cartilage, bones, and muscle of the ears and neck, a significant population of rhombomere 4-derived neural crest is fated to generate the glial component of the seventh cranial nerve.

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“…Cre , have been previously generated by insertion of the E. coli lacZ gene and of the Cre recombinase gene, respectively, into the Krox20 locus (Schneider-Maunoury et al, 1993;Voiculescu et al, 2000). In homozygous mutants, hindbrain segments, r3 and r5, are eliminated (Schneider-Maunoury et al, 1993, 1997Voiculescu et al, 2001), myelination is impaired in the peripheral nervous system (Topilko et al, 1994), and endochondral bone formation is affected (Levi et al, 1996).…”

Section: Krox20mentioning

confidence: 99%