Rensching cats and dogs: feeding ecology and fecundity trends explain variation in the allometry of sexual size dimorphism.

The tendency for sexual size dimorphism (SSD) to increase with body mass in taxa where males are larger, and to decrease when females are larger, is known as Rensch's rule. In mammals, where the trend occurs, it is believed to be the result of a competitive advantage for larger males, while female mass is constrained by the energetics of reproduction. Here, we examine the allometry of SSD within the Felidae and Canidae, demonstrating distinctly different patterns: in felids, there is positive allometric scaling, while there is no trend in canids. We hypothesize that feeding ecology, via its effect on female spacing patterns, is responsible for the difference; larger male mass may be advantageous only where females are dispersed such that males can defend access to them. This is supported by the observation that felids are predominately solitary, and all are obligate carnivores. Similarly, carnivorous canids are more sexually dimorphic than insectivores and omnivores, but carnivory does not contribute to a Rensch effect as dietary variation occurs across the mass spectrum. The observed inter-familial differences are also consistent with reduced constraints on female mass in the canids, where litter size increases with body mass, versus no observable allometry in the felids.

Binding to the yeast SwI4,6-dependent cell cycle box, CACGAAA, is cell cycle regulated in vivo.

In Saccharomyces cerevisiae commitment to cell division occurs late in the G1 phase of the cell cycle at a point called Start and requires the activity of the Cdc28 protein kinase and its associated G1 cyclins. The Swi4,6-dependent cell cycle box binding factor, SBF, is important for maximal expression of the G1 cyclin and HO endonuclease genes at Start. The cell cycle regulation of these genes is modulated through an upstream regulatory element termed the SCB (SwI4,6-dependent cell cycle box, CACGAAA), which is dependent on both SWI4 and SWI6. Although binding of SWI4 and SWI6 to SCB sequences has been well characterized in vitro, the binding of SBF in vivo has not been examined. We used in vivo dimethyl sulfate footprinting to examine the occupancy of SCB sequences throughout the cell cycle. We found that binding to SCB sequences occurred in the G1 phase of the cell cycle and was greatly reduced in G2. In the absence of either SWI4 or SWI6, SCB sequences were not occupied at any cell cycle stage. These results suggest that the G1-specific expression of SCB-dependent genes is regulated at the level of DNA binding in vivo.

Tetrahymena telomerase RNA levels increase during macronuclear development.

Telomeres, the G-rich sequences found at the ends of eukaryotic chromosomes, ensure chromosome stability and prevent sequence loss from chromosome ends during DNA replication. During macronuclear development in Tetrahymena, the chromosomes fragment into pieces ranging from 20 kb to 1,500 kb. Tetrahymena telomerase, a ribonucleoprotein, adds telomeric (TTGGGG)n repeats onto telomeres and onto the newly generated macronuclear DNA ends. We have investigated whether telomerase RNA levels increase during macronuclear development, since such an increase might be expected during chromosomal fragmentation. The steady-state level of the telomerase RNA component was used to estimate the abundance of telomerase present in mating and nonmating Tetrahymena. Northern blot analysis revealed that in vegetatively growing Tetrahymena, there were 18,000-40,000 copies of telomerase RNA per cell. In mating cultures, the levels of RNA increased 2- to 5-fold at 9-15 h, and 1.5- to 3.5-fold in starved nonmating cultures. This increase in telomerase RNA paralleled telomerase activity, which also increased slightly in mating and starved nonmating cells.

Telomerase primer specificity and chromosome healing.

Chromosome healing by de novo telomere addition at nontelomeric sites has been well characterized in several organisms. The Tetrahymena telomerase ribonucleoprotein uses an internal RNA template to catalyse d(TTGGGG)n telomere addition to the 3' end of telomeric sequence in vitro and in vivo. Studies of telomerase RNA indicated that hybridization of the RNA template region, 5'-CAACCCCAA-3', to the 3' end of single-stranded telomeric oligonucleotides might be important for primer recognition and utilization. The apparent requirement of telomerase for pre-existing telomeric sequence has raised questions regarding its role in chromosome healing. We report here that Tetrahymena telomerase can specifically elongate single-stranded DNA oligonucleotides whose termini are not complementary to the RNA template sequence 5'-CAACCCCAA-3'. These data suggest that telomerase may be able to heal chromosomes directly in vivo.

Effect of vitamin E on lifespan and reproduction in Caenorhabditis elegans.

Vitamin E extends the lifespan of many animals, including the nematode Caenorhabditis elegans. Our results confirm previous studies that 200 micrograms/ml vitamin E significantly prolonged C. elegans survival (17-23%, P less than 0.05) when added from hatching to day 3, while continuous exposure, either at hatching or from 4 days prior to hatching, had little additional effect. Treatment with 100 or 400 micrograms/ml vitamin E, or with other antioxidants (80 micrograms/ml vitamin C, either alone or in combination with vitamin E, or 120 micrograms/ml N,N'-diphenyl-1,4-diphenylenediamine (DPPD] did not significantly affect lifespan. All treatments with 200 micrograms/ml vitamin E moderately reduced fecundity (total progeny) and increased the mean day of reproduction. At 400 micrograms/ml, vitamin E had severe effects, while DPPD, vitamin C, and 100 micrograms/ml vitamin E had slight effects on both these parameters of reproduction. These data suggest that vitamin E increases lifespan in C. elegans in part by slowing development in the same manner that metabolic-depressant or mildly cytotoxic drugs increase lifespan, decrease fecundity, and delay the timing of reproduction.