Presented to the 16th Penn State Symposium in Plant Physiology, May 18-20, 2006,
Session on: Regulation of Gene Expression by RNA

Author to contact: John Frenster
Institution: Physicians’ Educational Series
E-mail: FrensterJH@aol.com

"Activator RNA Initiation of the DNA Transcription Bubble".

*John H  Frenster and Jeannette A. Hovsepian

Activator RNA Research, Physicians’ Educational Series,
Atherton, CA 94027-5446, USA

The DNA Strand-Separation model of eukaryotic gene regulation (1) is based on the ability of DNA and RNA sequences to interact during the initiation and elongation phases of selective DNA transcription. RNA-DNA helices are more stable than DNA-DNA helices, and RNA-RNA helices are still more stable (2). Activator RNA is capable of binding to complementary DNA sequences in the anti-template DNA strand, and by such binding is capable of opening the DNA-DNA helix at selective sites for the initiation of DNA transcription on the DNA-template strand. As premessenger RNA is synthesized on the DNA-template strand, RNA splicing results in the formation of excised RNA exons, RNA introns, and RNA 5' leader sequences (3). Such excised 5' leader RNA sequences are the complement of the activator RNA sequences that initiated the transcription process. When DNA transcription is excessive at a particular gene locus, rising levels of messenger RNA and of 5' leader RNA from that locus are produced by the splicing process. Such increased levels of 5' leader RNA, specific for the given gene locus, are now capable of binding to activator RNA at the gene locus. Since RNA-RNA helices are more stable than DNA-RNA helices, activator RNA may be removed from the anti-template DNA strand at the gene locus. Such loss of activator RNA from the gene locus may result in a decrease of DNA transcription at that locus, thus providing a feedback-loop for the control of RNA synthesis at a particular gene locus. The RNA-RNA complex formed by such feedback may be very stable, and may be capable of storage during oogenesis, passage to daughter cells during mitosis, and/or transport to other nearby cells during embryonic induction (4).

References: (at: http://www.euchromatin.net)

1. Frenster JH, "Mechanisms of Repression and De-Repression within Interphase Chromatin",
In Vitro: 1, 78-101 (1965).

2. Frenster JH, "Correlation of the Binding to DNA Loops or to DNA Helices with the Effect on RNA Synthesis", Nature:  208, 1093 (December 11, 1965).

3. Herstein PR, and Frenster JH, "Mated Models of Gene Regulation in Eukaryotes", in:
"Embryonic and Fetal Antigens in Cancer", vol. 2, pp. 5-7, Oak Ridge National Lab., Oak Ridge, Tenn., 1972.

4. Czihak G, "Evidence for Inductive Properties of the Micromere-RNA in Sea-urchin Embryos", Naturwissenschaften: 52, no. 6, 141-142 (1965).


Links to RNA and Biological Causality:

A Brief History of  Activator RNA:



Further Topics in:  Euchromatin,  active DNA, and  RNA  ribo-regulators:

Links to Euchromatin Activator RNA Reviews:
Links to Euchromatin Activator RNA Research:
Links to Ultrastructural Probes of DNase I-Sensitive Sites:
Links to RNA as a Therapeutic Agent:
Links to Hodgkin Lymphoma Immuno-Pathology:
Links to Activated T-Lymphocyte Immunotherapy:
Links to Medical Systems Biology:
Links to Selective Gene Transcription:
Links to RNA-Induced Epigenetics:
Links to RNA-Induced Embryogenesis:
Links to RNA and Biological Causality:
Links to Reprogramming and Neoplasia:

"Ultrastructural Probes of Active DNA Sites, and the RNA Activators of DNA".



Top of Page - Euchromatin Network - Current Research - Forums - Other Sites - Future Events -


For Further Information and Feedback:
Phone:  +1 650 367 6483
E-mail: frenster@euchromatin.net



euchromatin: "the most active portion of the genome within the cell nucleus".