GnRH, more basic than "unspecified" ste2,3

Teresa Binstock binstoct at essex.UCHSC.edu
Fri Mar 15 04:22:36 EST 1996

Richard offers the point that, if Patel et al's "undefined" [and 
unpublished] STE2 and STE3 are not labeling human thymic antigens 
homologous to S. Cerevisiae STE2 and STE3, then Teresa's hypothesis 
about sexual and gender orientaion is totally shot down. He makes his 
point clearly, after which I demonstrate the hypothesis to be alive and 

On 14 Mar 1996, Richard Aaron Warnock wrote:
> ...<much snipped>
> Here, you say that
> ste2 and ste3 are on human epithelium. This is based on your medline
> search with ste2 and ste3 as keywords that yielded:
> 1. Patel DD; Whichard LP; Radcliff G; Denning SM; Haynes BF.
>    Journal of Clinical Immunology, 1995 Mar, 15(2):80-92.
> ...ste2 and ste3 in that article refer to antibodies agaist *Surface Thymic
> Epithelium" undefined antigens, and not yeast alpha-receptors.
> Kinda blows apart the whole thing, eh?

Teresa responds that her S/O and G/O hypothesis is alive and well for the 
following reasons:

0. Whether or not Patel et al's STE2 and STE3 are labeling molecules 
homologous to S. cerevisiae STE2 and STE3 is not necessarily relevant. 

1. Yeast's alpha-factor is functionally homologous to mammalian GnRH.

2. GnRH and GnRH receptors are in the thymus and are expressed on 
T-cells; in other words, a mammalian functional-homologue of alpha-factor 
is present in the thymus and in T-cells.

3. Yeast's reception of alpha-factor affects cell cycle. At least one 
study thus far reports that mammalian GnRH affects cell cycle in T cells. 

4. Just as one class of yeast cells generally produces GnRH-like 
alpha-factor, so too do human T-cells produce GnRH.

5. Whether or not a-factor homologues exist in humans remains to be 
reported; what is clear is that the basic structure of a-factor molecules 
is quite similar to endogenous substances in humans.

In general, therefore, the fact that GnRH-receptors exist in the 
mammalian thymus indicates that molecules functionally akin to alpha-factor 
receptors exist in the mammalian thymus -- totally independently of what 
Patel et al were referring to via their use of the acronyms STE2 and STE3.

To move forwards, S. Cerevisiae has genes for both a- and alpha-factor 
pheromones and receptors, but generally expresses and utilizes only the 
appropriate pheromone and receptor combination. Similarly, male and 
female humans, amidst all their beyond-yeast complexity, have all the 
GnRH-capabilities enumerated hereinabove, but also have a more complex 
immune system than does S. Cerevisiae; thus (at least hypothetically) 
humans have more diverse ways whereby sex-identification alternatives 
(ie variations of sexual and/or gender orientation) could occur -- ie, 
by mechanisms like those of autoimmumity, but focused in relation to 
sexually significant chemo-signaling, as perceived in the nasal mucosa and 
possibly the epidermis.


Cites in support of the numbered statements:

TI  - Evidence that secretory products of the reticuloepithelial cells of
      the rat thymus modulate the secretion of gonadotrophins by rat
      pituitary cells in culture.
SO  - Journal of Reproductive Immunology 1995 Mar;28(3):203-15

TI  - Association of the yeast pheromone response G protein beta gamma
      subunits with the MAP kinase scaffold Ste5p.
SO  - Science 1995 Sep 15;269(5230):1572-5

TI  - Signal requirements for production of luteinizing hormone
      releasing-hormone by human T cells.
SO  - Cellular Immunology 1995 Jul;163(2):280-8

TI  - Coordinate gene expression of luteinizing hormone-releasing hormone
      (LHRH) and the LHRH-receptor after prolactin stimulation in the rat
      Nb2 T-cell line: implications for a role in immunomodulation and
      cell cycle gene expression.
SO  - Molecular Endocrinology 1995 Jan;9(1):44-53

TI  - Synthesis and biological activity of fluorescent yeast pheromones.
SO  - Biochemistry 1995 Mar 21;34(11):3553-60

TI  - Neonatal treatment with luteinizing hormone-releasing hormone
      analogs alters peripheral lymphocyte subsets and cellular and
      humorally mediated immune responses in juvenile and adult male
SO  - Journal of Clinical Endocrinology & Metabolism 1994 Feb;78(2):292-8

TI  - Alterations in thymic and bone marrow lymphocyte subpopulations in
      GnRH agonist treated prepubertal female mice.
SO  - Journal of Reproductive Immunology 1993 Nov;25(2):167-84

TI  - Thymus-neuroendocrine-liver pathway.
SO  - Medical Hypotheses 1993 Nov;41(5):470-2

TI  - Immunoactivation enhances the concentration of luteinizing
      hormone-releasing hormone peptide and its gene expression in human
      peripheral T-lymphocytes.
SO  - Endocrinology 1993 Jul;133(1):215-23

TI  - Functional homology of protein kinases required for sexual
      differentiation in Schizosaccharomyces pombe and Saccharomyces
      cerevisiae suggests a conserved signal transduction module in
      eukaryotic organisms.
SO  - Molecular Biology of the Cell 1993 Jan;4(1):107-20

TI  - Thymocytes express a mRNA that is identical to hypothalamic
      luteinizing hormone-releasing hormone mRNA.
SO  - Cellular & Molecular Neurobiology 1992 Oct;12(5):447-54

TI  - Yeast mating pheromone activates mammalian gonadotrophs:
      evolutionary conservation of a reproductive hormone?.
SO  - Science 1982 Dec 24;218(4579):1323-5

TI  - Effect of gonadotrophin releasing hormone in underfed immature rats.
SO  - Indian Journal of Physiology & Pharmacology 1981 Oct-Dec;25(4):374-8

TI  - Luteinizing hormone-releasing hormone signaling at the lymphocyte
      involves stimulation of interleukin-2 receptor expression.
SO  - Endocrinology 1991 Jul;129(1):277-86

TI  - A physiological role for the neuropeptide luteinizing
      hormone-releasing hormone (LHRH) during the maturation of thymus
      gland function.
SO  - International Journal of Neuroscience 1990 Apr;51(3-4):287-9

TI  - Luteinizing hormone-releasing hormone (LHRH) agonist restoration of
      age-associated decline of thymus weight, thymic LHRH receptors, and
      thymocyte proliferative capacity.
SO  - Endocrinology 1989 Aug;125(2):1037-45


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