Stanford Advisors

All Publications

  • Context-dependent expression of the foraging gene in field colonies of ants: the interacting roles of age, environment and task. Proceedings. Biological sciences / The Royal Society Ingram, K. K., Gordon, D. M., Friedman, D. A., Greene, M., Kahler, J., Peteru, S. 2016; 283 (1837)


    Task allocation among social insect workers is an ideal framework for studying the molecular mechanisms underlying behavioural plasticity because workers of similar genotype adopt different behavioural phenotypes. Elegant laboratory studies have pioneered this effort, but field studies involving the genetic regulation of task allocation are rare. Here, we investigate the expression of the foraging gene in harvester ant workers from five age- and task-related groups in a natural population, and we experimentally test how exposure to light affects foraging expression in brood workers and foragers. Results from our field study show that the regulation of the foraging gene in harvester ants occurs at two time scales: levels of foraging mRNA are associated with ontogenetic changes over weeks in worker age, location and task, and there are significant daily oscillations in foraging expression in foragers. The temporal dissection of foraging expression reveals that gene expression changes in foragers occur across a scale of hours and the level of expression is predicted by activity rhythms: foragers have high levels of foraging mRNA during daylight hours when they are most active outside the nests. In the experimental study, we find complex interactions in foraging expression between task behaviour and light exposure. Oscillations occur in foragers following experimental exposure to 13 L : 11 D (LD) conditions, but not in brood workers under similar conditions. No significant differences were seen in foraging expression over time in either task in 24 h dark (DD) conditions. Interestingly, the expression of foraging in both undisturbed field and experimentally treated foragers is also significantly correlated with the expression of the circadian clock gene, cycle Our results provide evidence that the regulation of this gene is context-dependent and associated with both ontogenetic and daily behavioural plasticity in field colonies of harvester ants. Our results underscore the importance of assaying temporal patterns in behavioural gene expression and suggest that gene regulation is an integral mechanism associated with behavioural plasticity in harvester ants.

    View details for DOI 10.1098/rspb.2016.0841

    View details for PubMedID 27581876

    View details for PubMedCentralID PMC5013789

  • Influence of nuclear structure on the formation of radiation-induced lethal lesions INTERNATIONAL JOURNAL OF RADIATION BIOLOGY Friedman, D. A., Tait, L., Vaughan, A. T. 2016; 92 (5): 229-240


    Purpose The rejoining of fragmented nuclear DNA caused by ionizing radiation may lead to lethal chromosome rearrangements, such as rings or dicentrics. The clinically useful linear quadratic relationship between dose and cell survival has been interpreted as the generation of lethal lesions secondary to damage occurring in two separate chromosomes simultaneously (α component), or as potentially repairable separate events (β component). Here, the generation of such lesions is discussed, synthesizing existing knowledge with new insights gleaned from spatial proximity data made possible by high-throughput sequencing of chromosome conformation capture experiments. Over a range of several Mbp, the linear DNA strand is organized as a fractal globule generating multiple sites of contact that may facilitate deletions or inversions if the points of contact are damaged. On a larger scale, transcriptionally active euchromatin occupies a physically identifiable space separate from inactive areas and is preferentially susceptible to free radical attack after irradiation. Specific transcriptional programs link genomic locations within that space, potentially enhancing their interaction if subject to simultaneous fragmentation by a single radiation event. Conclusions High throughput spatial analysis of the factors that control chromosome proximity has the potential to better describe the formation of the lethal chromosome aberrations that kill irradiated cells.

    View details for DOI 10.3109/09553002.2016.1144941

    View details for Web of Science ID 000375624000001

    View details for PubMedID 26917327

  • Could ehrlichial infection cause some of the changes associated with leukemia, myelodysplastic diseases and autoimmune disorders, and offer antibiotic treatment options? Medical hypotheses Kallick, C. A., Friedman, D. A., Nyindo, M. B. 2015; 85 (6): 891-893


    We hypothesize that a large group of medical conditions of unknown etiology including leukemia, multiple myeloma, myelodysplastic and autoimmune disorders, may be associated with or caused by an obscure group of intracellular obligate parasitic bacteria named Ehrlichia/Anaplasma (EA). Ensconced in the stem cells of the bone marrow, EA may disrupt the normal development and function of many of the cells of immunity, manifesting itself as different syndromes. Recent studies of the activity of EA suggest direct effects on the immune system consistent with the manifestations of leukemia. We reference here three leukemia patients with direct or indirect evidence of EA infection. Moreover, EA have been shown to be most sensitive to rifamycins. Two moribund leukemia patients with levels of platelets and white cells incompatible with life were treated with therapeutic doses of Rifampin. Though they did not survive, their condition improved dramatically for a time, suggesting Rifampin provided some therapeutic benefit. We assert that these results warrant more extensive study.

    View details for DOI 10.1016/j.mehy.2015.09.015

    View details for PubMedID 26394545

  • Large-Scale Coding Sequence Change Underlies the Evolution of Postdevelopmental Novelty in Honey Bees MOLECULAR BIOLOGY AND EVOLUTION Jasper, W. C., Linksvayer, T. A., Atallah, J., Friedman, D., Chiu, J. C., Johnson, B. R. 2015; 32 (2): 334-346


    Whether coding or regulatory sequence change is more important to the evolution of phenotypic novelty is one of biology's major unresolved questions. The field of evo-devo has shown that in early development changes to regulatory regions are the dominant mode of genetic change, but whether this extends to the evolution of novel phenotypes in the adult organism is unclear. Here, we conduct ten RNA-Seq experiments across both novel and conserved tissues in the honey bee to determine to what extent postdevelopmental novelty is based on changes to the coding regions of genes. We make several discoveries. First, we show that with respect to novel physiological functions in the adult animal, positively selected tissue-specific genes of high expression underlie novelty by conferring specialized cellular functions. Such genes are often, but not always taxonomically restricted genes (TRGs). We further show that positively selected genes, whether TRGs or conserved genes, are the least connected genes within gene expression networks. Overall, this work suggests that the evo-devo paradigm is limited, and that the evolution of novelty, postdevelopment, follows additional rules. Specifically, evo-devo stresses that high network connectedness (repeated use of the same gene in many contexts) constrains coding sequence change as it would lead to negative pleiotropic effects. Here, we show that in the adult animal, the converse is true: Genes with low network connectedness (TRGs and tissue-specific conserved genes) underlie novel phenotypes by rapidly changing coding sequence to perform new-specialized functions.

    View details for DOI 10.1093/molbev/msu292

    View details for Web of Science ID 000350050700004

    View details for PubMedID 25351750

  • Commentary: Portuguese crypto-Jews: the genetic heritage of a complex history. Frontiers in genetics Marcus, A. W., Ebel, E. R., Friedman, D. A. 2015; 6: 261-?

    View details for DOI 10.3389/fgene.2015.00261

    View details for PubMedID 26300912

    View details for PubMedCentralID PMC4528994