Accurate transcription of mouse metallothionein-I gene in a fractionated nuclear extract from a rat hepatoma.

نویسندگان

  • K A Maguire
  • M L Webb
  • L C Garg
  • S T Jacob
چکیده

Nuclear extract from Morris hepatoma 3924A was fractionated by DEAE-Sephadex chromatography. The fraction eluting with 300 mM (NH4)2SO4 (DE-C) was used for transcribing cloned mouse metallothionein-I (MT-I) gene in a run-off assay. This fraction contained the majority of RNA polymerase II as well as the transcription factor(s). Accuracy of MT-I DNA transcription was confirmed by S1 nuclease mapping. Low concentrations (1 microgram/ml) of alpha-amanitin inhibited the reaction, indicating that RNA polymerase II directed the transcription. Unfractionated nuclear extracts from the hepatoma or a rat mammary adenocarcinoma as well as whole cell extract obtained from the mammary tumor also transcribed MT-I gene. The extent of transcriptional activity was in the following order: hepatoma nuclear fraction DE-C greater than whole cell extract derived from rat mammary adenocarcinoma cells greater than nuclear extract derived from rat hepatoma or rat mammary adenocarcinoma cells. These studies have demonstrated that a fractionated nuclear extract obtained from a tissue supports efficient and accurate RNA polymerase II-mediated transcription of MT-I DNA.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Suppression of metallothionein-I/II expression and its probable molecular mechanisms.

Metallothionein (MT) promoter was methylated in rat hepatoma and in mouse lymphosarcoma cells by methylation of cytosine within the CpG dinucleotide region. After demethylation of MT-I promoter in mouse lymphosarcoma cells or in the transplanted rat hepatoma with 5-azacytidine, a potent inhibitor of DNA methyltransferase, the promoter was activated in response to heavy metal treatment. MT-I pro...

متن کامل

Gene Expression under F8 Promoter Driving In Mouse Hepatoma Cells: A Step towards Gene Therapy of Hemophilia

Background and Objectives: Significant progress has been made in treatment of hemophilia. Ex-vivo gene therapy is going popular due to the capability of this method in using isogenic cells for genetic manipulation and reintroducing them into same host after proliferation. Most gene therapy techniques use viral vectors, which usually harbor a strong and non-specific promoter (e...

متن کامل

Post - transcriptional regulation of messenger abundance in rat Bver and hepatorru

Saturation hybridisation with labelled single—copy UTA shows that polysomal poly(A)+ HHA of rat liver and of a minimus—deviation rat hepatcma cell—line (HTC) have similar total complexities and that few sequenoes are specific to either coil-type. Hybridisation kinetios of polygonal olKls with tenplate and heterologous oell RHAB indioate that • proportion of liver messengers are at greatly reduc...

متن کامل

I-51: The Role of the Transcription FactorGCNF in Germ Cell Differentiation and Reproductionin Mice

The germ cell nuclear factor (GCNF) is a member of the nuclear receptor super family of transcription factors. GCNF expression during gastrulation and neurulation is critical for normal embryogenesis in mice. GCNF represses expression of the POU domain transcription factor Oct4 during mouse post-implantation development in vivo. Oct4 is thus down-regulated during female gonadal development, whe...

متن کامل

Negative regulation of catalase gene expression in hepatoma cells.

For an understanding of the molecular basis of the marked decrease in catalase activity of various tumor cells, expression of the catalase gene was studied in rat and human hepatoma cell lines and in rat liver, which was used as a control with high activity. RNA blot hybridization profiles and run-on assays indicated that the decrease in catalase activity was due to depression of catalase gene ...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • The Journal of biological chemistry

دوره 262 9  شماره 

صفحات  -

تاریخ انتشار 1987