The development of health protective behaviors among college students.

This study uses structural equation modeling and a panel design to explain participation in health protective behavior (HPB) among college students. The direct, indirect, and total effects of gender, social influences (parental and peer behavior), social attachments (activity involvement, social support, and romantic involvement), social triggers (personal health, acute illnesses, and personal or family health crisis), health value, and effort to improve health behavior on HPB are examined. A path model with a high goodness of fit and an R2 of .418 shows that gender; health value, and effort to change health behaviors are the most powerful predictors of HPB participation, while parents and peers influence HPB indirectly through influence on health value and effort to change. Neither the social attachment nor social trigger items influenced HPB in this sample. Implications of these findings are discussed.

On the development of ectopic eyes in Drosophila melanogaster produced by the mutation extra eye (ee).

The mutation ee often produces an ectopic eye on the vertex that is a mirror image partial duplication of the normal eye on the ipsilateral side of the head. The pattern of the duplication and a clonal analysis by mitotic recombination indicate that the duplications are of dorsal eye and orbital structures. Large ectopic eyes (more than 100 ommatidia) and their surrounding bristles may be produced without cuticular deficiencies. The penetrance of ee is temperature dependent with penetrance higher (72%) at 25 degrees and 29 degrees than at 19 degrees (43%). Temperature shift experiments show two temperature-sensitive periods: one at midembryogenesis, the other at mid-first larval instar. Microscopic examination of ee late-second and third instar imaginal cephalic discs show no indication of growth of the extra tissue needed to produce the duplication until after mid-third instar. This was confirmed by cell counts of ee and wild-type discs. There is no evidence of differential cell death in the two types of discs at this stage, although much earlier cell death is postulated. Tests for cell autonomy of the mutation by the production of morphogenetic clones suggest nonautonomy. Formation of pattern duplications by mutant genes is discussed in terms of cell death that eliminates whole developmental compartments, restricted cell death that occurs within a compartment, extensive cell death within a compartment and proliferative growth unassociated with cell lethality.

Evolution of the Alpha-Esterase Duplication within the Montana Subphylad of the Virilis Species Group of Drosophila.

Previous studies on linkage disequilibrium involving four tightly linked genes that code for the alpha-esterases of Drosophila montana suggest that these loci arose from a primitive esterase gene by gene duplication, followed by tandem duplication (Roberts and Baker 1973). We have examined the esterase variants in the closely related species, lacicola, flavomontana and borealis. These studies reveal that borealis has only a single esterase locus, and flavomontana may have only two loci. Cytological studies, using aceto-orcein staining and Hoechst fluorescence of squashes of ganglion chromosomes, reveal acrocentric Y chromosomes for all six species of the montana phylad, with the exception of borealis, which has the primitive rod-shaped Y chromosome. These studies provide evidence against the hypothesis (Stone, Guest and Wilson 1960) that borealis and flavomontana are derived from montana, but support Throckmorton's (1978) conclusion of the early divergence of the former two species. This phylogenetic relationship supports our contention that the difference in the number of esterase genes with active alleles between borealis and montana is based on an increase in the number of genes coding for the alpha-esterases, rather than the retention in borealis of three genes with null alleles.

A fine-structure gynandromorph fate map of the Drosophila head.

A gynandromorph fate map of the head of D. melanogaster was produced using 28 landmarks derived from one imaginal disc. An examination of the meaning of fine-structure mapping discloses that the sturt value observed between one pair of landmarks within a disc may approximate the relative physical distance of their progenitor cells at blastoderm, but for another pair of landmarks (assuming no directed cell movements), the sturt value may simply reflect their close geographic location at the time the cells are specified for their particular differentiation, a time much later in development when most cell division within the disc has come to an end. The formation of early developmental compartments has little effect on fate-map distances. Our analysis of the data suggests there are approximately ten cells present at the blastoderm stage that are head progenitors. Each blastoderm cell is likely to be the progenitor of a particular array of landmarks, but there is overlap between arrays from different blastoderm cells.

Linkage disequilibrium over space and time in natural populations of Drosophila montana.

The previously described allelic frequencies and linkage disequilibrium among the active and null alleles of four tightly linked loci coding for the alpha-esterases were found to be maintained by one population for 5 years, and were found to be present in two other populations which were shown to be genetically distinct from the first. It appears that enzyme variants coded by these highly polymorphic loci are being maintained in the populations by selective forces.

Evidence for position-effect suppression of the ribosomal RNA cistrons in Drosophila melanogaster.

Unambiguous evidence is presented that two X-chromosome inversions produce lethality in X/O males because of position-effect suppression of genes in the basal heterochromatin. The data support the hypothesis that the ribosomal RNA cistrons are the genes suppressed. There is evidence for a region in the X basal heterochromatin that may act as a regulator of rDNA activity.