Description
Springer New Frontiers In The Study Of Gene Functions 1987 Edition by George Poste, Stanley T. Crooke
The heat-shock proteins in E. coli are transiently overexpressed af ter shift to a higher growth temperature. The genes that encode the HSPs are preceded by promoters transcribed in vitro by a form of RNA poly 32 32 merase holoenzyme containing a 32-kd a subunit (Ea ). The a subunit is encoded by the rpoH (htpR) gene, previously identified as a positive 32 effector of the heat-shock response. Our evidence suggests that Ea is the enzyme that transcribes heat-shock genes at all temperatures. The level 32 of a may be regulated at several points: Accumulation of rpoH mRNA 32 is affected by temperature shift, a synthesis is regulated posttranscrip 32 tionally, and a is an unstable molecule with a tl/2 of 5 min. Many mu tations in the HSPs are shown to have defects in proteolysis. References Baker. T. A. , Grossman. A. D . . and Gross. C. A. , 1984, A gene regulating the heat shock response in Escherichia coli also affects proteolysis. Proc. Natl. A cad. Sci. US. A. 81:6779-6783. Bardwell, J. C. A . . and Craig, E. A . . 1984. Major heat shock gene of Drosophila and the Escherichia coli heat-inducible dnaK gene are homologous, Proc. Natl. Acad. Sci. US. A. 81:848-852. Bukhari. A. I. . and Zipser. D . . 1973, Mutants of Escherichia coli with a defect in the degradation of nonsense fragments, Nature New Bioi. 243:238-241. Charette. M. F. , Henderson, G. W. , and Markovitz, A. Table of contents : 1 The Role of Cis- and Trans-Acting Functions in Simian Virus 40 Gene Regulation.- 1. Introduction.- 2. Early Viral Transcriptional Program.- 3. Late Viral Transcriptional Program.- 4. Discussion.- References.- 2 Regulation of the Heat-Shock Response in Escherichia coli.- 1. Introduction.- 2. Transcription of the Heat-Shock Genes.- 3. Regulation of rpoH and ?32.- 4. Function of the Heat-Shock Proteins.- 5. Summary.- References.- 3 Negative Control of DNA Replication Revealed in Composite Simian Virus 40-Bovine Papillomavirus Plasmids.- 1. Overview.- 2. Introduction.- 3. Results.- 3.1. Construction of Composite Simian Virus 40-Bovine Papillomavirus Replicons.- 3.2. Construction of Permanent Cell Lines Containing Simian Virus 40-Bovine Papillomavirus Composite Plasmids.- 4. Discussion.- 4.1. Negative Control of DNA Replication.- 4.2. Mechanisms of Replication Control.- 4.3. Gene Amplification.- 4.4. Relation to the Inactive Mating-Type Cassettes in Yeast.- References.- 4 DNA Supercoiling as a Regulator of Bacterial Gene Expression.- 1. Introduction.- 2. Results and Discussion.- References.- 5 Retrotransposition in Yeast.- 1. Introduction.- 2. Experiments.- 3. Speculation.- References.- 6 Comparative Genetic Analysis of Homeobox Genes in Mouse and Man.- 1. Introduction.- 2. Murine Homeobox Genes.- 3. Human Homeobox Genes.- 4. Comparative Genetic Relationships between Species.- 5. Comparative Genetic Relationships within Species.- 6. Possible Functional Relationships between Homeobox Loci and Linked Genes.- 6.1. Mouse Hox-1, Chromosome 6.- 6.2. Mouse Hox-2, Chromosome 11.- 6.3. Mouse Hox-3, Chromosome 15.- 6.4. Human Hox-1, Chromosome 7.- 6.5. Human Hox-2, Chromosome 17.- 7. Discussion.- References.- 7 Eukaryotic Transcriptional Specificity Conferred by DNA-Binding Proteins.- 1. Introduction.- 2. Results and Discussion.- 2.1. Cis and Trans Regulatory Components of the Simian Virus 40 Promoter.- 2.2. Role of Sp1 in Other Viral and Cellular Promoters.- 2.3. A Consensus Sp1 Recognition Sequence.- 3. Concluding Remarks.- References.- 8 Chromatin Structure Near an Expressed Gene.- 1. Introduction.- 2. Results.- 3. Discussion.- References.- 9 Specificity of Gene Expression and Insertional Mutagenesis in Transgenic Mice.- 1. Introduction.- 2. Experiments and Results.- 2.1. Spatial and Temporal Control of Marker Gene Expression in Mice Carrying ?A Crystallin-Chloramphenicol Acetytransferase, ?2(I) Collagen-Chloramphenicol Acetyltransferase, or Rous Sarcoma Virus-Chloramphenicol Acetyltransferase Chimeric Genes.- 2.2. Dominant Lens Tumors Caused by an ?A Crystallin-Simian Virus 40 Large-T Antigen Fusion Gene.- 2.3. Syndactyly in a Rous Sarcoma Virus-Chloramphenicol Acetyltransferase Strain.- References.- 10 Retroviruses as Insertional Mutagens.- 1. Introduction.- 2. Insertion of Moloney Murine Leukemia Viruses into the Germ Line of Mice.- 3. Expression of the Proviral Genome in Mov Substrains of Mice.- 4. Induction of Two Insertional Mutations.- 5. Insertional Mutagenesis by Retroviruses and DNA Injection.- References.- 11 P Transposable Elements and Their Use as Vectors for Gene Transfer in Drosophila.- 1. Introduction.- 2. Results and Discussion.- 2.1. A Strategy for the Analysis of P-Element Functions.- 2.2. All Four P-Element Open Reading Frames Are Required for Transposase Activity.- 2.3. Tissue Specificity of P-Element Transposition.- 2.4. P-Element-Encoded Proteins.- References.- 12 Mapping and Manipulating Immunoglobulin Functions.- 1. Introduction.- 2. Immunoglobulin Gene and Protein Structure.- 3. Production of Monoclonal Immunoglobulins from Mouse and Man.- 4. Uses of Specific Immunoglobulins.- 5. Optimizing Immunoglobulin Structure for Therapy.- 6. Identifying the Molecular Requirements for Immunoglobulin Synthesis and Function.- 7. Future Studies on the Structural and Regulatory Mutants.- References.- 13 T4: A T-Cell Surface Protein Mediating Cell-Cell and Cell-AIDS Virus Interactions.- 1. Introduction.- 2. Results.- 2.1. Isolation of Complementary DNAs That Encode Both T4 and T8.- 2.2. Nucleotide Sequences of T4 and T8.- 2.3. Evolution of T4 and T8.- 2.4. T4 Expression Is Required for AIDS Virus Infection.- 2.5. Infection by AIDS Is Not Restricted to T Lymphocytes.- 2.6. T4 Serves as a Receptor for AIDS Virus.- 2.7. Receptor-Mediated Endocytosis: A Possible Mechanism of Viral Entry.- References.- 14 Identifying the Determinants of Protein Function and Stability.- 1. Introduction.- 2. Repressor and Cro Background.- 2.1. Protein Structures.- 2.2. Complexes with Operator DNA.- 3. Isolation of Phenotypically Defective Mutants.- 4. Structural Distribution of Mutant Sites.- 5. Why Are Mutant Proteins Nonfunctional?.- 5.1. Contribution of Proteolysis to Mutant Phenotypes.- 5.2. Mutations That Affect Protein Stability.- 5.3. DNA-Binding Mutations.- 6. Phenotypic Reversion.- 6.1. Same-Site Revertants.- 6.2. Second-Site Revertants.- 6.3. Suppression Occurs by Enhancement of Activity.- 7. Summary.- References.