FUNCTION OF MAMMALIAN SINGLE MINDED GENES, SIM1 AND SIM2
FUNCTION OF MAMMALIAN SINGLE MINDED GENES, SIM1 AND SIM2
批准号:
6182659
负责人:
CHEN-MING FAN
金额:
$21.51万
依托单位国家:
美国
项目类别:
财政年份:
1998
资助国家:
美国
项目状态:
已结题
起止时间:
1998-05-01 至 2003-04-30
关键词:
Drosophilidae biochemical evolution developmental genetics developmental neurobiology disease /disorder model early embryonic stage gene expression gene targeting genetic enhancer element genetic mapping genetic promoter element genetically modified animals histology immunocytochemistry in situ hybridization laboratory mouse nucleic acid sequence phenotype protein purification tissue /cell culture
中文摘要
描述(改编自研究者摘要):本研究的目标
目的是研究哺乳动物Sim1和Sim2基因的功能
使用转基因小鼠模型。 Sim1和Sim2是
果蝇sim基因。 在飞行中,SIM扮演着重要的角色
在中枢神经系统的发展中起着重要作用。 的初步研究
小鼠Sim基因强烈提示进化上保守的功能。
SIM蛋白含有称为PAS结构域的保守序列基序,
它被几种环境传感器蛋白共享,例如二恶英
受体,缺氧诱导因子,果蝇昼夜节律
调节器Per和B。枯草芽孢杆菌芽孢形成调节因子KinA。 这
信息强烈表明,西姆斯也可以响应特定的
环境信号通过其PAS域。 该提案包括
以下目的:1)记录Sim1和Sim2在
2)建立缺乏Sim1和Sim2基因功能的小鼠模型,
同源重组和表征突变体表型,
评估这些基因的正常功能,3)识别可能的小
调节Sim1和Sim2功能的分子配体。 重要的是,
小鼠Sim2基因位于同线人类唐氏综合征关键基因中,
地区 此外,缺乏Sim1的突变小鼠表现出神经系统
可能与多发性硬化症有关的疾病。 探索和
鉴定调节Sim1和Sim2可能的小配体
功能将是开发方法以改变其功能的第一步。
体内基因活性。
英文摘要
DESCRIPTION (adapted from investigator's abstract): The goal of this
proposal is to investigate the function of mammalian Sim1 and Sim2 genes
using transgenic mouse models. Sim1 and Sim2 are homologues of the
Drosophila sim (singleminded) gene. In the fly, sim plays essential roles
in the development of the central nervous system. Preliminary studies of
the mouse Sim genes strongly suggest evolutionarily conserved functions.
The SIM proteins contain conserved sequence motif termed the PAS domain,
which is hared by several environmental sensor proteins such as the Dioxin
receptor, the Hypoxia Inducible Factor, the Drosophila circadian rhythm
regulator Per, and the B. subtilis sporulation regulator KinA. This
information strongly indicated that SIMs may also respond to specific
environmental signals via their PAS domains. This proposal includes the
following aims: 1) documenting the expression patterns of Sim1 and Sim2 in
detail; 2) establishing mouse models lacking Sim1 and Sim2 gene function by
homologous recombination and characterizing mutant phenotypes in order to
assess the normal function of these genes, and 3) identifying possible small
molecule ligands that modulate the function of Sim1 and Sim2. Importantly,
the mouse Sim2 gene is located in the syntenic human Down syndrome critical
region. Furthermore, mutant mice lacking Sim1 display neurological
disorders that may relate to multiple sclerosis. Exploration and
identification of possible small ligands that regulate Sim1 and Sim2
function will be the first step towards developing methods to alter their
gene activities in vivo.
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