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J Tower

Publications and source records attributed to J Tower.

10 recordsLinked to original sources
PubMed1990

Genetics of 51D-52A, a region containing several maternal-effect genes and two maternal-specific transcripts in Drosophila.

Two genomic clones exhibiting a maternal-specific pattern of expression map to cytological region 52A. To elucidate the function of these clones we have undertaken a mutagenesis of the cytological region 51D-52A. This paper presents the results of this screen and the preliminary analysis of female-sterile and lethal mutations isolated. A total of twelve complementation groups have been identified, four of which are defined exclusively by female-sterile alleles. Only one visible mutation was isolated, a recessive temperature-sensitive allele of Thickened-arista (Tarts). Several of the seven lethal loci display an embryonic lethal phase. Three of the four female-sterile loci affect chorion structure with one resulting in underamplification of the chorion genes, and two (possibly three) of the four female-steriles affect nuclear division/DNA replication. Thus it appears that this is a "developmentally important" region, possibly representing a clustering of genes involved in either DNA replication or nuclear division.

Alleles↗
PubMed1989

An RNA polymerase I promoter located in the CHO and mouse ribosomal DNA spacers: functional analysis and factor and sequence requirements.

We report results of experiments in which we demonstrated the existence of a polymerase I promoter within the ribosomal DNA spacer upstream from the rRNA initiation site in Chinese hamsters and mice. Transcription of the CHO spacer promoter was achieved by the same protein factors, C and D, that catalyzed transcription of the gene promoter, and these factors bound stably to the CHO spacer promoter in a preinitiation complex, just as they did to the gene promoter. In contrast to the CHO spacer promoter, which was transcribed in vitro nearly as efficiently as the gene promoter, the mouse spacer promoter was far less active; this low activity was attributable to the fact that the mouse spacer promoter bound factor D inefficiently. It is striking that the active CHO spacer promoter violated the otherwise universal rule that metazoan RNA polymerase I promoters all have a G residue at position -16. Sequence comparisons also revealed a great similarity between the CHO and mouse spacer promoter regions, yet there was much less similarity between the flanking sequences. There was also only limited homology between the spacer and gene promoter regions, but despite this the two kinds of initiation regions were organized similarly, both consisting of an essential core promoter domain and a stimulatory domain that extended upstream to approximately residue -135. Evolutionary considerations argue strongly that the presence of ribosomal DNA spacer promoters offers a significant selective advantage.

Animals↗
PubMed1988

Polymerase III transcription factor B activity is reduced in extracts of growth-restricted cells.

Extracts of cells that are down-regulated for transcription by RNA polymerase I and RNA polymerase III exhibit a reduced in vitro transcriptional capacity. We have recently demonstrated that the down-regulation of polymerase I transcription in extracts of cycloheximide-treated and stationary-phase cells results from a lack of an activated subform of RNA polymerase I which is essential for rDNA transcription. To examine whether polymerase III transcriptional down-regulation occurs by a similar mechanism, the polymerase III transcription factors were isolated and added singly and in pairs to control cell extracts and to extracts of cells that had reduced polymerase III transcriptional activity due to cycloheximide treatment or growth into stationary phase. These down-regulations result from a specific reduction in TFIIIB; TFIIIC and polymerase III activities remain relatively constant. Thus, although transcription by both polymerase III and polymerase I is substantially decreased in extracts of growth-arrested cells, this regulation is brought about by reduction of different kinds of activities: a component of the polymerase III stable transcription complex in the former case and the activated subform of RNA polymerase I in the latter.

Animals↗
PubMed1987

Transcription of mouse rDNA is regulated by an activated subform of RNA polymerase I.

We have identified the species-nonspecific factor required for mouse rDNA transcription, factor C, as an activated subform of RNA polymerase I. C is an RNA polymerase I since it copurifies with bulk polymerase I activity on the three chromatographic columns used to achieve a virtually homogenous preparation of polymerase I, as well as on four additional matrices; it is quantitatively neutralized as well as immunoprecipitated by two different types of anti-polymerase I antibodies; and it has thermal lability identical to that of bulk polymerase I. However, C is clearly distinct from bulk polymerase I in its ability to participate in the stable rDNA transcription complex and to catalyze accurate initiation of rRNA synthesis. It also has a greater sedimentation coefficient than bulk polymerase I. Furthermore, this activated polymerase subform is specifically lacking in extracts of cells in which rDNA transcription was down-regulated because of cycloheximide treatment or attainment of stationary phase. These data suggest that regulation of rDNA transcription in vivo may involve modulation in availability of the activated polymerase I subform.

Animals↗
PubMed1986

Factors and nucleotide sequences that direct ribosomal DNA transcription and their relationship to the stable transcription complex.

We have studied the protein components and nucleic acid sequences involved in stably activating the ribosomal DNA (rDNA) template and in directing accurate transcription of mammalian rRNA genes. Two protein components are necessary to catalyze rDNA transcription, and these have been extensively purified. The first, factor D, can stably associate by itself with the rDNA promoter region and is responsible for template commitment. The second component, factor C, which appears to be an activated subset of polymerase I, can stably bind to the factor D-rDNA complex but not to the rDNA in the absence of factor D. A third component which had been previously identified as a rDNA transcription factor is shown to be a RNase inhibitor. Extending our earlier observation that the approximately 150-base-pair mouse rDNA promoter consists of a minimal essential region (residues approximately -35 to approximately +9) and additional upstream stimulatory domains, we now report that each of these promoter domains acts to augment the binding of the polymerase I transcription factors. A minimum core region (residues approximately -35 to approximately -15) is capable of stable complex formation and of binding transcription factor D. Factor C can also bind to this D-core region complex.

Animals↗
PubMed1985

A complex control region of the mouse rRNA gene directs accurate initiation by RNA polymerase I.

To determine the size and location of the mouse rDNA promoter, we constructed systematic series of deletion mutants approaching the initiation site from the 5' and 3' directions. These templates were transcribed in vitro under various conditions with S-100 and whole-cell extracts. Surprisingly, the size of the rDNA region that determines the level of transcription differed markedly, depending on the reaction conditions. In both kinds of cell extracts, the apparent 5' border of the promoter was at residue ca. -27 under optimal transcription conditions, but as reaction conditions became less favorable, the 5' border moved progressively out to residues -35, -39, and -45. The complete promoter, however, extends considerably further, for under other nonoptimal conditions, we observed major effects of promoter domains extending in the 5' direction to positions ca. -100 and -140. In contrast, the apparent 3' border of the mouse rDNA promoter was at residue ca. +9 under all conditions examined. We also show that the subcloned rDNA region from -39 to +9 contains sufficient information to initiate accurately and that the region between +2 and +9 can influence the specificity of initiation. These data indicate that, although the polymerase I transcription factors recognize and accurately initiate with only the sequences downstream of residue -40, sequences extending out to residue -140 greatly favor the initiation reaction; presumably, this entire region is involved in rRNA transcription in vivo.

Animals↗