第一节 癌基因 Oncogenes 第二节 肿瘤抑制基因 tumor suppressor gene 第三节 生长因子 Growth factors

6.1 遗传信息的概念 6.2基因表达调控的理论与模式 6.2.1.2 stringent response control 6.2.1.3 基因表达调控的综合实例 6.2.1.4 Attenuator control CΔ E L.S. — D C B A 0 16.5 6.2.2 post-transcriptional level control 6.2.2.1 pre-RNA processing 6.2.2.2 Anti sense RNA (micRNA) 6.2.2.2 anti-sense RNA control protein translation 6.2.2.3 RNA interference (RNAi )的发现与证实 6.2.2.4 microRNA (miRNA) 6.2.3 Translational level control 6.2.3.1 Operon内各基因以一定比例的协调翻译 6.2.3.2 Modulate—codon usage & tRNA 6.2.3.3 Informasome 6.2.3.4 蛋白质合成的自体调控 6.2.3.5 mRNA 二级结构对翻译的调节 6.2.3.6 可逆性磷酸化对转录与翻译过程的调节 6.2.3.7 mRNA 的结构对翻译水平的调控 6.2.4 Gene expression control 6.2.4.1 蛋白质分泌的信号肽假说 6.2.4.2 protein degradation 6.3 表观遗传及其分子机制 Epigenetic and Molecular Mechanism 6.3.1 ATP－dependent Chromatin remodeling

基因定位 gene location 连锁分析(linkage analysis) 体细胞杂交法（somatic cell hybridization） 克隆嵌板法（clone panel method） 原位杂交（in situ hybridization） 荧光原位杂交（florescence in-situ hybridization,FISH） 基因定位的应用 人类基因组计划

第一节 基因诊断的概念及常用技术 第二节 基因诊断策略 第三节 基因诊断的应用前景 第四节 遗传病的基因诊断 第五节 肿瘤的基因诊断 第六节 感染性疾病的基因诊断 一、基因治疗的策略 二、基因转移技术 四、治疗基因的受控表达 三、基因干预 五、基因治疗的应用研究

Muscle cells But if in the same organIsm, should have the same DNA per Nerve cells( cell Different cells have different clusters of genes active Development and differentiation of embryos is controlled by signaling molecules that alter gene expression in cells

How p53 and Rb pathway function may be disrupted in cancer cells Components of the pathway which are found altered in human cancers are shown in red on the diagram above p53 and Rb themselves may be inactivated by gene mutation (loss of both copies or also as in familial retinoblastoma and Li-Fraumeni syndrome where there are inherited mutations in one copy of Rb or p53 gene respectively. Alternatively

Operon fusion: transcriptional – Promoter from foreign gene – Translational sequence from reporter gene

17.1 Introduction 17.2 The mating pathway is triggered by pheromone-receptor interactions 17.3 The mating response activates a G protein 17.4 Yeast can switch silent and active loci for mating type 17.5 The MAT locus codes for regulator proteins 17.6 Silent cassettes at HML and HMR are repressed 17.7 Unidirectional transposition is initiated by the recipient MAT locus 17.8 Regulation of HO expression 17.9 Trypanosomes switch the VSG frequently during infection 17.10 New VSG sequences are generated by gene switching 17.11 VSG genes have an unusual structure 17.12 The bacterial Ti plasmid causes crown gall disease in plants 17.13 T-DNA carries genes required for infection 17.14 Transfer of T-DNA resembles bacterial conjugation 17.15 Selection of amplified genomic sequences 17.16 Transfection introduces exogenous DNA into cells 17.17 Genes can be injected into animal eggs 17.18 ES cells can be incorporated into embryonic mice 17.19 Gene targeting allows genes to be replaced or knocked out

Gene clusters are formed by duplication and divergence Sequence divergence is the basis for the evolutionary clock Pseudogenes are dead ends of evolution Unequal crossing-over rearranges gene clusters Genes for rRNA form tandem repeats ( The repeated genes for rRNA maintain constant sequence) Crossover fixation could maintain identical repeats Satellite DNAs often lie in heterochromatin Arthropod satellites have very short identical repeats Mammalian satellites consist of hierarchical repeats Minisatellites are useful for genetic mapping

29.1 Introduction 29.2 Fly development uses a cascade of transcription factors 29.3 A gradient must be converted into discrete compartments 29.4 Maternal gene products establish gradients in early embryogenesis 29.5 Anterior development uses localized gene regulators