MOLECULAR GENETIC CONTROL OF OLIGODENDROCYTE DEVELOPMENT
MOLECULAR GENETIC CONTROL OF OLIGODENDROCYTE DEVELOPMENT
批准号:
6363923
负责人:
Mengsheng Qiu
金额:
$19.45万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2000
资助国家:
美国
项目状态:
已结题
起止时间:
2000-03-01 至 2004-02-28
关键词:
Retroviridae brain cell differentiation cell growth regulation chick embryo developmental genetics developmental neurobiology embryo /fetus cell /tissue gene expression gene induction /repression gene mutation homeobox genes laboratory mouse molecular genetics mutant neurogenesis oligodendroglia phenotype spinal cord transfection /expression vector
中文摘要
描述(逐字摘要):这项研究的长期目标是
了解少突胶质细胞的分子和遗传控制
规范和差异化。最近,三个 Nkx 同源盒基因 Nkx-6.1,
Nkx-6.2 和 Nkx-2.2 已被鉴定为特异性表达于
腹侧脊髓中的少突胶质细胞前体细胞。此外,
这三个 Nkx 基因的表达也可以在分化过程中检测到。
或胚胎发生后期的成熟少突胶质细胞。于是,就已经
假设 Nkx 基因在控制
少突胶质细胞的规范、分化或成熟。四具体
这里提出的目标是检验这一假设并系统地
表征 Nkx 基因在少突胶质细胞控制中的功能
发展。目标 1 是表征少突胶质细胞表型
Nkx-2.2突变小鼠。目标 2 是研究 Nkx-6.2 的效果
少突胶质细胞分化的突变。目标 3 是研究
Nkx-2.2 和 Nkx-6.2 双突变体中少突胶质细胞的发育
研究它们在控制少突胶质细胞中可能的冗余作用
发展。目标4是测试Nkx-6.1、Nkx-6.2和Nkx-6.2的效果
通过过表达这些来异位表达对少突胶质细胞分化的影响
使用鸡胚胎背脊髓中的基因
有复制能力的禽逆转录病毒作为基因传递系统。测试
需要三个 Nkx 基因同时表达的可能性
少突胶质细胞诱导,我们将研究少突胶质细胞的发育
Pax-6 突变体,其中 Nkx-2.2 表达在
Nkx-6.1 和 Nkx-6.2 域。因此,心室前体细胞
Nkx-2.2 和 Nkx-6.1 共表达,Nkx-6.2 也在背侧扩展
Pax-6 突变体和少突胶质细胞前体结构域可能符合
向背侧延伸。
拟议研究的结果将显着增强我们的能力
了解控制早期规范的遗传电路和
少突胶质细胞的分化,并可为设计提供理论依据
预防和治疗运动神经元的新治疗方法
和少突胶质细胞萎缩。
英文摘要
DESCRIPTION (Abstract verbatim): The long-term goal of this study is
to understand the molecular and genetic control of oligodendrocyte
specification and differentiation. Recently, three Nkx homeobox genes, Nkx-6.1,
Nkx-6.2 and Nkx-2.2, have been identified that are specifically expressed in
the oligodendrocyte precursor cells in the ventral spinal cord. In addition,
expression of these three Nkx genes can also be detected in the differentiating
or mature oligodendrocytes at late stages of embryogenesis. Thus, it has been
hypothesized that the Nkx genes play important roles in controlling the
specification, differentiation or maturation of oligodendrocytes. Four specific
aims are proposed here to test this hypothesis and to systematically
characterize the function of the Nkx genes in the control of oligodendrocyte
development. Aim 1 is to characterize the oligodendrocyte phenotypes in the
Nkx-2.2 mutant mice. Aim 2 is to investigate the effects of the Nkx-6.2
mutation on oligodendrocyte differentiation. Aim 3 is to study the
oligodendrocyte development in the Nkx-2.2 and Nkx-6.2 double mutants to
investigate their possible redundant role in controlling the oligodendrocyte
development. Aim 4 is to test the effects of Nkx-6.1, Nkx-6.2 and Nkx-6.2
ectopic expression on oligodendrocyte differentiation by overexpressing these
genes in the dorsal spinal cord of chicken embryos using the
replication-competent avian retrovirus as a gene delivery system. To test the
possibility that simultaneous expression of three Nkx genes is required for
oligodendrocyte induction, we will study the oligodendrocyte development in the
Pax-6 mutants, in which the Nkx-2.2 expression is dorsally expanded within
the Nkx-6.1+ and Nkx-6.2+ domain. Thus, the ventricular precursor cells
coexpressing Nkx-2.2 and Nkx-6.1, Nkx-6.2 is also dorsally expanded in the
Pax-6 mutants and oligodendrocyte precursor domain might be according
extended dorsally.
Results derived from the proposed studies will significantly enhance our
understanding of the genetic circuitry governing the early specification and
differentiation of oligodendrocytes, and may provide theoretic basis for design
of novel therapeutic approaches for prevention and treatment of motor neuron
and oligodendrocyte atrophies.
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