|Deloof, Arnold - CATHOLIC UNIV, BELGIUM|
|Hakim, Raziel - HOWARD UNIV WASHINGTON DC|
|Jaffe, Howard - NAT. INST. OF HEALTH|
|Schoofs, Lilliane - CATHOLIC UNIV, BELGIUM|
|Steel, Colin - YORK UNIV. ONTARIO CANDA|
Submitted to: Archives of Insect Biochemistry and Physiology
Publication Type: Review Article
Publication Acceptance Date: May 4, 2001
Publication Date: N/A
Interpretive Summary: Unlocking the secrets of the reproductive physiology of pest species of moths is important to knowing how to disrupt and prevent their reproduction. This review article discusses the discovery that the testes make an insect steroid hormone, ecdysteroid, and that the synthesis of the hormone is dependent upon activation by a peptide from the brain. The brain npeptide, LTE, was isolated and its structure was described. In addition, the mechanism of LTE signalling action was determined. An antibody to LTE indicated that an LTE-like material was present in particular parts of the brain and nerve cord, indicating the areas of synthesis and possible transport to the testes. Within the testes, LTE immunoreactivity was found in the outer sheath. LTE immunoreactivity was also found in other developing organs, indicating that it may have a wider role than just stimulation of ecdysteroid synthesis. Ecdysteroid in the testis promotes production of a growth factor, also synthesized by the testis sheaths, which stimulates development and maturation of the male genital tract. Therefore, LTE is very important in controlling development of the male lepidopteran reproductive system. Drugs that inhibit LTE synthesis or action will disrupt the reproductive potential of pest insects and will be useful in population control. The information in this article can be used by other scientists interested in male insect reproductive physiology.
Technical Abstract: Testes of lepidoptera synthesized ecdysteroid in a somewhat different temporal pattern than the prothoracic glands that release ecdysteroid to the hemolymph. Brain extracts from Heliothis virescens and Lymantria dispar induced testes to synthesize ecdysteroid, but did not affect prothoracic glands. The testis ecdysiotropin (LTE) was isolated from L. dispar pupal brains by a series of high pressure chromatography steps. It' sequence was Ile-Ser-Asp-Phe-Asp-Glu-Tyr-Glu-Pro-Leu-Asn-Asp-Ala-Asp-Asn -Asn-Glu-Val-Leu-Asp-Phe-OH, of molecular mass 2,473 Daltons. The predominant signaling pathway for LTE was via Gi protein, IP3, diacylglycerol and PKC; a modulating pathway, apparently mediated by an angiotensin II-like peptide, was controlled via Gs protein, cAMP and PKA. Testis ecdysteroid caused isolated testis sheaths to also synthesize a growth factor that induced development of the male genital tract. The growth factor appeared to be a glycoprotein similar to vertebrate alpha-1 -glycoprotein. A polyclonal antibody to LTE indicated LTE-like peptide in the medial neurosecretory cells of the brain, the suboesophageal and other ganglia, and also in its target organ, the testis sheath. However, LTE-like activity was also detected in optic lobes, antennae, frontal ganglia and elongating spermatids of developing L. dispar pupae. This may indicate that LTE has a role in development as well as stimulation of testis ecdysteroid synthesis. Key words: Male reproduction, neuropeptide, ecdysteroid, cell signalling, immunocytochemistry.