Slow Growth and Increased Spontaneous Mutation Frequency in Respiratory Deficient afo1- Yeast Suppressed by a Dominant Mutation in ATP3

A yeast deletion mutation in the nuclear-encoded gene, AFO1, which codes for a mitochondrial ribosomal protein, led to slow growth on glucose, the inability to grow on glycerol or ethanol, and loss of mitochondrial DNA and respiration. We noticed that afo1- yeast readily obtains secondary mutations that suppress aspects of this phenotype, including its growth defect. We characterized and identified a dominant missense suppressor mutation in the ATP3 gene. Comparing isogenic slowly growing rho-zero and rapidly growing suppressed afo1- strains under carefully controlled fermentation conditions showed that energy charge was not significantly different between strains and was not causal for the observed growth properties. Surprisingly, in a wild-type background, the dominant suppressor allele of ATP3 still allowed respiratory growth but increased the petite frequency. Similarly, a slow-growing respiratory deficient afo1- strain displayed an about twofold increase in spontaneous frequency of point mutations (comparable to the rho-zero strain) while the suppressed strain showed mutation frequency comparable to the repiratory-competent WT strain. We conclude, that phenotypes that result from afo1- are mostly explained by rapidly emerging mutations that compensate for the slow growth that typically follows respiratory deficiency

Developmental asynchrony and host species identity predict variability in nestling growth of an obligate brood parasite: a test of the “growth-tuning” hypothesis

Generalist obligate brood parasites are excellent models for studies of developmental plasticity, as they experience a range of social and environmental variation when raised by one of their many hosts. Parasitic Brown-headed Cowbirds (Molothrus ater (Boddaert, 1783)) exhibit host-specific growth rates, yet cowbird growth rates are not predicted by hosts’ incubation or brooding periods. We tested the novel “growth-tuning” hypothesis which predicts that total asynchrony between cowbirds’ and hosts’ nesting periods results in faster parasitic growth in nests where host young fledge earlier than cowbirds. We tested this prediction using previously-published and newly-added nestling mass data across diverse host species. Total nesting period asynchrony (summed across incubation and brooding stages) predicted cowbird growth; 8-day old cowbirds were heavier in host nests with relatively shorter nesting periods. We further explored the drivers of variation in growth using mass measurements of cowbirds in Song Sparrow (Melospiza melodia (Wilson, 1810)) and Red-winged Blackbird (Agelaius phoeniceus (Linnaeus, 1766)) nests. Our top models included host species (cowbirds grew faster in sparrow nests), numbers of nestmates (slowest when raised alone), and sex (males grew faster). These results confirm that multiple social and environmental factors predict directional patterns of developmental plasticity in avian generalist brood parasites.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Parasitic cowbirds may defeat host defense by causing rejecters to misimprint on cowbird eggs

Experiments suggest that some hosts that reject parasitic brown-headed cowbird (Molothrus ater) eggs develop egg recognition by imprinting on their own eggs, probably at the first nest naïve birds attend. This raises the possibility that parasitism of naïve individuals might cause them to mistakenly misimprint on, and accept, cowbird eggs. In an egg-learning experiment designed to cause misimprinting, hosts accepted cowbird eggs when they had laid only 1 egg even though most rejected cowbird eggs when nests had ≥2 host eggs. These findings show that cowbirds can cause misimprinting by parasitizing naïve hosts. If done opportunistically, misimprinting should become more likely as cowbird abundance increases. In accord with this expectation, simulated brood parasitism showed that 3 host species that usually reject cowbird eggs were more tolerant of cowbird eggs in the Great Plains, where cowbirds reach maximal historic abundance, than in eastern North America where cowbirds are less common. This relation between parasite abundance and host responses is opposite to that found in cuckoo hosts. In addition, these 3 rejecter species had high rates (10.8--30.4%) of natural cowbird parasitism at an Illinois site where cowbirds are extremely, and historically, abundant. These rejecters accepted most cases of researcher-detected parasitism, even though they rarely accept where cowbirds are less common. Despite the potentially high cost resulting from egg rejection, we demonstrate that parasitism of "rejecters" can be adaptive for cowbirds particularly when host egg recognition involves learning. Copyright 2009, Oxford University Press.