Born:

South Bend, Indiana

Education:

B.S., Biology, University of Notre Dame, 1962 Ph.D. Entomology, Purdue University, 1966

Professional:

Professor of Entomology, Texas A&M University 1966 - 2003

Professor Emeritus 2004

TEACHING:

ENTO 306 (Undergraduate) Insect Physiology

ENTO 615 (Graduate) Insect Physiology

My research interests concerned insect hormones and their regulations of intermediary metabolism. My primary research focus was on the neurohormones and their regulatory actions on energy metabolism and reproduction. The long-range goal of the research was to identify physiological events unique to insects that might be sensitive to disruption for purposes of insect pest management.

My early research investigated the neuroendocrine regulation of metabolism in the insect fat body. The fat body is an insect tissue that is functionally similar to the vertebrate liver. It serves as a storage site for excess nutrients, as the major tissue for intermediary metabolism and as a source for the blood proteins, carbohydrates and lipids.

Using the tropical cockroach Blaberus discoidalis as a model, it was found that a neurohormone from the corpora cardiaca stimulates the basal metabolism of the insect with the fat body as its target tissue (Keeley and Friedman, 1967). The neurohormone appeared to exert its action on the mitochondria during a time when the mitochondria were showing a developmental maturation, shortly after the adult molt (Keeley, 1976). The fat body mitochondriogenesis occurs shortly after the adult molt when the tissue is undergoing maturation from an immature tissue - that stores nutrient materials - to a mature adult tissue capable of active biosynthetic activity (Keeley, 1981). The neurohormone appears to enhance the biosynthesis of hemes for mitochondrial cytochromes during mitochondriogenesis in the fat body by increasing aminolevulinic acid biosynthesis (Keeley, 1987). We later isolated and characterized the hypertrehalosemic hormone, a new insect neuropeptide hormone, that elevates trehalose, the major carbohydrate in insect hemolymph (Hayes et al, 1986). This short (10 amino acids) peptide also stimulated the biosynthesis of cytohemes a and b during the fat body mitochondriogenesis.

We also found that the hypertrehalosemic hormone stimulated the synthesis of a new insect cytochrome P450 (CYP4C1) that belongs to a family of P450s involved in fatty acid w-hydryoxylation. The action of the hypertrehalosemic hormone occurs at the level of expression of the CYP4C1 gene.

My later research investigated the endocrine regulations of vitellogenesis and colony founding in queens of the imported fire ant, Solenopsis invicta. Fire ant queens undergo a mating flight then break off their wings (dealation) almost immediately after returning to the ground. Shortly thereafter, the flight muscles begin to degenerate, and the amino acids that result from the digested proteins are used by the queen to form a first generation of eggs to produce tiny workers called nanitics. The nanitics care for and feed the queen and take care of a second generation of larvae (brood) that will produce more workers for development of the colony. The events of dealation, flight muscle degeneration and egg formation are endocrine regulated, presumably by the juvenile hormone.

We isolated and characterized a gene for vitellogenin and the gene for vitellogenin receptor.  The product of the gene we isolated was a constitutively expressed vitellogenin, one of three that are now known.  Vitellogenin is the precursor for the yolk protein. Vitellogenin is synthesized by the fat body, released and transported by the hemolymph to the developing oocyte. The vitellogenin binds to the vitellogenin receptor on the oocyte membrane and is carried into the oocyte where it is deposited in yolk granules to form vitellin, the yolk protein. The synthesis of vitellogenin is stimulated by the juvenile hormone, a product of an insect endocrine gland called the corpora allata. The juvenile hormone stimulates vitellogenin gene expression in the fat body to initiate the synthesis of vitellogenin. The juvenile hormone also may stimulate water loss and shrinkage by the ovarian follicle cells that surround the oocyte. The shrinkage of the follicle cells exposes the oocyte membrane to the hemolymph which carries the vitellogenin. The vitellogenin receptor can then bind the vitellogenin for transport into the developing oocyte and yolk formation. Hormones may also stimulate the oocytes to express the vitellogenin receptor gene for production of the receptor in preparation for yolk formation. It is also believed that the flight muscle histolysis may be initiated by juvenile hormone. In this case, the hormone may initiate events related to apoptosis (programmed cell death). The exact identification of the hormones controlling these actions is not confirmed and the mechanisms involved remain undefined.

Awards and Publications