help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Endocrinology, doi:10.1210/endo-125-3-1119
Endocrinology Vol. 125, No. 3 1119-1120
Copyright © 1989 by the Endocrine Society.
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by O'Malley, B. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by O'Malley, B. W.

Editorial: Did Eucaryotic Steroid Receptors Evolve from Intracrine Gene Regulators?*

Bert W. O'Malley

Abstract

It is likely that evolution of the steroid receptor superfamily of gene regulators began a thousand million years ago in very primitive organisms. Such organisms would have lacked cellular specialization (glands) and an endocrine system as such. Their needs were simple: 1) to survive in the environment and 2) to replicate. They were dependent on their environment for metabolic substrates and energy sources. Their prime regulatory need was to control their own metabolism. Classical steroid hormones were nonexistent. Although admittedly hypothetical, I suggest the following evolutionary scenario. Primitive members of the steroid receptor superfamily were intracellular receptors which bound environmental nutritional agents and/or metabolic substrates (e.g. amino acids or sugars) and by-products as ligands. These ligands were nonsteroidal in nature, with the possible exception of cholesterol. It is not inconceivable that certain of these intracellular receptors were activated by amino acids or other peptides. The ligands were likely to be absorbed from the environment or produced within the same cells which contained these receptors, thereby providing apparent constitutive activity. An exception would be times of metabolic deprivation when endogenous ligand concentration may have dropped. In this case the receptors would have become inactivated and gene expression shut down. Under normal conditions, however, the ligand pools would be used to modulate metabolic pathways and control cell division.

Footnotes

* Dr. O'Malley, the author of this editorial, is Professor and Chairman of Cell Biology at Baylor College of Medicine. He is a previous president of The Endocrine Society. (Individuals who wish to contribute editorials to Endocrinology should contact the Editor-in-Chief.)

Received June 16, 1989.




This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
N. Bhattacharyya, K. Pechhold, H. Shahjee, G. Zappala, C. Elbi, B. Raaka, M. Wiench, J. Hong, and M. M. Rechler
Nonsecreted Insulin-like Growth Factor Binding Protein-3 (IGFBP-3) Can Induce Apoptosis in Human Prostate Cancer Cells by IGF-independent Mechanisms without Being Concentrated in the Nucleus
J. Biol. Chem., August 25, 2006; 281(34): 24588 - 24601.
[Abstract] [Full Text] [PDF]


Home page
J EndocrinolHome page
A J W Hsueh, P Bouchard, and I Ben-Shlomo
Hormonology: a genomic perspective on hormonal research
J. Endocrinol., December 1, 2005; 187(3): 333 - 338.
[Abstract] [Full Text] [PDF]


Home page
J. Histochem. Cytochem.Home page
T. Iwasaka, S. Umemura, K. Kakimoto, H. Koizumi, and Y. R. Osamura
Expression of Prolactin mRNA in Rat Mammary Gland During Pregnancy and Lactation
J. Histochem. Cytochem., March 1, 2000; 48(3): 389 - 396.
[Abstract] [Full Text]


Home page
HypertensionHome page
R. Re
The Nature of Intracrine Peptide Hormone Action
Hypertension, October 1, 1999; 34(4): 534 - 538.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1989 by The Endocrine Society