THE ENDOCRINE BASIS OF PAIR-FORMATION BEHAVIOUR IN THE MALE EIDER SOMATERIA MOLLISSIMA

Pair-formation behaviour among the Eiders began after the annual moult, in late September. There was a small peak of display in October and November and a large one in the following April and May. As a result, the female population became paired in two phases, up to 50% in the autumn and the remainder in the following spring. The seasonal cycle of the abundance of Leydig cells was bimodal, with a peak in October and a large one in April-May. That the peaks represent increased androgen production was supported by the cycles of Leydig cell enzyme activity and lipid content and of penis weight. The monthly means of Leydig cell abundance and of the rate of display were statistically correlated. Experiments with sexually quiescent males in eclipse plumage demonstrated that testosterone was capable of inducing pair-formation behaviour. Relatively advanced stages of spermatogenesis were found in autumn, and were maintained through the winter, complete development occurring in the spring. Seasonal changes in the production of pituitary gonadotropin followed a bimodal pattern with peaks in autumn and in the spring. Field evidence is presented which suggests that Follicle Stimulating Hormone and Luteinizing Hormone were produced at different phases of a circadian rhythm of photosensitivity.     

Polyproline binding is an essential function of human profilin in yeast.

Structural analysis of human profilin has revealed two tryptophan residues, W3 and W31, which interact with polyproline. The codons for these residues were mutated to encode phenylalanine and the mutant proteins overexpressed in Eschericia coli. The isolated proteins were diminished in their ability to bind polyproline, whereas phosphatidylinositol 4,5-bisphosphate (PIP2) binding remained unchanged. In many strains of Saccharomyces cerevisiae, disruption of the gene encoding profilin, PFY1, is lethal. It was found that expression of the gene for human profilin is capable of suppressing this lethality. The polyproline-binding mutant alleles of the human gene were cloned into various yeast expression vectors. Each of the mutant genes resulted in suppression of the lethality of pfy1Delta. It was observed that the mutant protein expression levels paralleled the growth rates of the strains. The severity of various morphological abnormalities of the strains was also attenuated with increased protein levels, suggesting that profilin polyproline-binding mutations are deleterious to cell growth unless overexpressed. Both tryptophan mutations were combined to give a third mutant allele that was found both unable to bind polyproline and to suppress the lethality of a pfy1 deletion. Immunoprecipitation experiments suggested that the mutants were unaltered in their affinity for actin and PIP2. These data strongly suggest that polyproline binding is an essential function of profilin.     

The exosome of Trypanosoma brucei.

The yeast exosome is a complex of at least 10 essential 3'-5' riboexonucleases which is involved in 3'-processing of many RNA species. An exosome-like complex has been found or predicted to exist in other eukaryotes but not in Escherichia coli. The unicellular parasite Trypanosoma brucei diverged very early in eukaryotic evolution. We show here that T.brucei contains at least eight exosome subunit homologs, but only a subset of these associate in a complex. Accordingly, the T.brucei exosome is smaller than that of yeast. Both free and complex-associated homologs are essential for cell viability and are involved in 5.8S rRNA maturation. We suggest that the exosome was present in primitive eukaryotes, and became increasingly complex during subsequent evolution.