GENE AND TRANSGENE REGULATION IN THE DEVELOPING MOUSE

小鼠LIM-homeobox基因参与中枢神经系统发育 和神经内分泌组织。 该基因家族编码调节因子， 在图案形成和细胞发育中起关键作用 在后生动物发育过程中的规范。其产品含有两个N- 末端富含半胱氨酸的基序，LIM结构域，和相邻的 同源结构域 这个小组已经克隆并测序了 非洲爪蟾基因XLIM 1、XLIM 2和XLIM 3。同源性的程度是 非常高。 LIM 1在发育中的小鼠胚胎中的表达开始于 原肠胚形成，然后从胃肠道进入中枢神经系统， 端脑通过脊髓，并在发展中的排泄 系统 LIM 3基因在发育中的脑垂体中表达， 腹侧后脑和腹侧脊髓。 LIM 2的模式 目前正在调查中。 此外，删除两个 已经在小鼠生殖系中产生了鼠LIM基因 研究它们在小鼠发育过程中的作用机制。 人p53基因表达对小鼠透镜发育的影响。 野生的- 型人p53基因导致小眼症时，针对发展中国家 胚胎透镜的转基因小鼠。这种表型是由于 在出生后不久就开始的二次纤维分化。 通过 相反，透镜的发育几乎不受表达的影响。 DNA结合受损的突变型人p53。 表型引起的 野生型人p53基因的突变可以被突变等位基因拯救， 可能是通过显性负干扰的机制。 结果 对患者的p53基因治疗方案有意义。 D1 A多巴胺缺乏突变小鼠纹状体功能的改变 受体。 缺失纯合子小鼠携带D1 A纹状体神经元 完全没有功能性D1 A受体的细胞。 动物会死 断奶后不久，除非他们的饮食中补充了水分， 食物 虽然运动似乎不受影响，但小鼠表现出 饲养行为明显减少。 参与的细节 D1 A多巴胺受体在帕金森病发病机制中的作用 精神分裂症，以及它们在可卡因和安非他明成瘾中的作用， 在这种小鼠品系的帮助下进行了分析。

Murine LIM-homeobox genes involved in the development of central nervous and neuroendocrine tissues. This gene family encodes regulators of development that play pivotal roles in pattern formation and cell specification during metazoan development. Their products contain two N- terminal cysteine-rich motifs, the LIM domains, and an adjacent homeodomain. This group has cloned and sequenced murine homologs of the Xenopus laevis genes XLIM1, XLIM2 and XLIM3. The degree of homology is very high. LIM1 expression in the developing mouse embryo begins during gastrulation and later homes in on the central nervous system from the telencephalon through the spinal cord, and on the developing excretory system. The LIM3 gene is expressed in the developing pituitary gland, in the ventral hindbrain and the ventral spinal cord. The pattern of LIM2 expression is currently under investigation. Also, deletions in two murine lim genes have been generated in the mouse germline in an effort to study their mechanism of action during mouse development. Effects of human p53 expression on murine lens development. The wild- type human p53 gene causes microphthalmia when targeted to the developing embryonic lens in the transgenic mouse. This phenotype is due to a defect in secondary fiber differentiation that sets in shortly after birth. By contrast, lens development is almost unaffected by the expression of a mutant human p53 that is impaired in DNA binding. The phenotype caused by the wild-type human p53 gene can be rescued by the mutant allele, possibly via a mechanism of dominant negative interference. The results have implications for schemes of p53 gene therapy in patients. Altered striatal functions in a mutant mouse lacking D1A dopamine receptors. Mice homozygous for the deletion carry D1A striatal neurons that are totally devoid of functional D1A receptors. The animals die shortly after weaning unless their diet is supplemented with hydrated food. Although locomotion appears unaffected, the mice display a significant decrease in rearing behavior. Details of the involvement of D1A dopamine receptors in the pathogenesis of Parkinson's disease and schizophrenia, and their role in cocaine and amphetamine addiction can be analyzed with the help of this mouse strain.