Faculty available to advise comps: Camill,
Hougen-Eitzman, McKone, Rand, Singer, Tymoczko, Walser-Kuntz, Wolff, and Zweifel 

1. (Camill – fall/spring only) With the decline in populations worldwide, interest has grown in determining whether nature reserves and marine protected areas (MPAs) are able to stabilize populations and maintain biodiversity. What ecological factors must be considered when designing reserves or MPAs, and how well do they work?

Prendergast J.R., R.M. Quinn, and J.H. Lawton 1999. The gaps between theory and practice in selecting nature reserves. Conservation Biology 13: 484-492.

Halpern, B.S. 2003. The impact of marine reserves: do reserves work and does reserve size matter? Ecological Applications 13:S117-S137.

Roberts, C., S. Andelman, G. Branch, R. Bustamante, J.C. Castilla, J. Dugan, B. Halpern, H. Leslie, K. Lafferty, J. Lubchenco, D. McArdle, H. Possingham, M. Ruckleshaus, and R. Warner. 2003. Ecological criteria for evaluating candidate sites for marine reserves. Ecological Applications 13:S199-S214.

2. (Camill – fall/spring only) Because boreal and Arctic soils store roughly the same amount of carbon as the atmosphere, there is concern that climate warming and permafrost thaw will lead to a release of trace gases, such as carbon dioxide and methane, and accelerate climate warming. Evaluate the literature to determine how trace gas flux from northern ecosystems may change as climate warms.

Gorham, E. 1991. Northern peatlands – role in the carbon-cycle and probable responses to climatic warming. Ecological Applications 1:182-195.

Melillo J. M., P.A. Steudler, J. D. Aber, K. Newkirk, H. Lux, F. P. Bowles, C. Catricala, A. Magill, T. Ahrens, and S. Morrisseau. 2002. Soil warming and carbon-cycle feedbacks to the climate system. Science 298:2173-2176

Hobbie, S. E. 1996. Temperature and plant species control over litter decomposition in Alaskan tundra. Ecological Monographs 66:503-522

Oechel W. C., G. L. Vourlitis, S. J. Hastings, SJ, R. C. Zuleta, L. Hinzman, and D. Kane. 2000. Acclimation of ecosystem CO2 exchange in the Alaskan Arctic in response to decadal climate warming. Nature 406:978-981

3. (Walser-Kuntz – winter/spring only) Infection by a virus induces an antiviral immune response in the host. A successful response controls viral replication and leads to elimination of the virus. Not to be outdone, viruses have evolved several evasive strategies that allow them to persist despite the defense system of the host. Explore the mechanisms behind both the host defense response and the evasion strategy of the virus

Iannello, A., O. Debbeche, E. Martin, L. H. Attalah, S. Samarani, and A. Ahmad. 2006. Viral strategies for evading antiviral cellular immune responses of the host. Journal of Leukocyte Biology 79:16-35

4. (Tymoczko) Exercise is known to affect a host of biochemical processes including muscle growth, mitochondria biogenesis, response to insulin, altered immune response amongst others. The details of these effects remain to be determined. Investigate one of the effects of exercise and propose a biochemical exAs planation for the physiological response.

References for this question will be available soon.

5. (Wolff – winter/spring only; Jaramillo) Both pluripotent and committed (multipotent) stem cells have recently received attention in scientific and popular media for their potential therapeutic properties. However, the primary role of stem cells is to provide a renewable source of cells for development and maintenance of tissues. Multipotent neural stem cells (NSCs) give rise to both neurons and glia during embryonic development and, in many cases, throughout the life of an organism. Recent studies have revealed that a population of cells previously thought to be committed glia act as NSCs in embryos and adults. Other studies provide evidence that NSCs play roles in learning and memory, aging, growth of brain tumors, and evolution of the mammalian cortex.

Examine our current understanding of and propose possible mechanisms for neural stem cell maintenance and function 1) during embryonic development, or 2) in the adult nervous system, or 3) in disease progression.

Aimone J. B., J. Wiles, and F. H. Gage. 2006. Potential role for adult neurogenesis in the encoding of time in new memories. Nature Neuroscience 9: 723-7

Kriegstein A., S. Noctor, and V. Martinez-Cerdeno. 2006. Patterns of neural stem and progenitor cell division may underlie evolutionary cortical expansion. Nature Reviews Neuroscience 7:883-90

Merkle F. T., and A. Alvarez-Buylla. 2006. Neural stem cells in mammalian development. Current Opinion in Cell Biology 18:704-9

Vescovi A. L., R. Galli, and B. A. Reynolds. 2006. Brain tumour stem cells. Nature Reviews Cancer 6:425-36

6. (Zweifel – student submitted question) In the medical literature the term ‘mitochondrial disorders’ is applied to the clinical syndromes associated with abnormalities in oxidative phosphorylation (OXPHOS). Since the respiratory chain is formed by a collaboration of the nuclear genome and the mitochondrial genome, mitochondrial disorders include both mendelian-inherited and cytoplasmic-inherited diseases. Examine the relationship between the mitochondrial genotype and the phenotype of these human diseases.

Wallace, D.C. 2005. A mitochondrial paradigm of metabolic and degenerative diseases, aging, and cancer: A dawn for evolutionary medicine. Annual Review of Genetics 39:359-407

Taylor, R. W., and Turnbull, D. M. 2005. Mitochondrial DNA mutations in human disease. Nature Reviews Genetics 6:389-402

7. (Zweifel; Singer – Fall/Winter only) A major tenet of Mendelian genetics is that the parental origin of an allele does not affect its function in the F1 generation. For the vast majority of genes this still holds true. However, experiments and pedigree anlaysis have uncovered convincing evidence of exceptions to this general rule for some genes in mammals. The phenomenon in which a gene’s expression depends on the parent that transmits it is known as genomic imprinting. Discuss the identification and characterization of imprinted genes, and the possible molecular mechanisms underlying this unique form of epigenetic regulation.

Schaefer C.B., S. K. Ooi, T. H. Bestor, and D. Bourc’his. 2007. Epigenetic decisions in mammalian germ cells. Science 316:398-9

Munshi A., and S. Duvvuri. 2007 Genomic imprinting – the story of the other half and the conflicts of silencing. Journal of Genetics and Genomics 34:93-103

8. (Hougen-Eitzman) Warning signals and mimicry are widespread in nature. As posited by Darwin and Wallace, these traits presumably evolved to provide protection from other species. The signals can involve some type of visual or chemical mimicry (such as Batesian and Müllerian mimicry), as well as a warning signal (aposematic coloration). Even though these types of signals are commonly studied, it is often unclear both how they might have evolved and their exact ecological function. Examine the evolution or ecological basis of a signal that helps the user gain protection from attack.

Darst, C. A., M.E. Cummings, and D. C. Cannatella. 2006. A
mechanism for diversity in warning signals: Conspicuousness versus
toxicity in poison frogs. Proceedings of the National Academy of
Sciences 103:5852–5857

Beatty, C. C., K Beriinckx, and T. N. Sherratt. 2004. The evolution of mullerian mimicry in multispecies communities. Nature 431:63-67

Lambardi, D., R. R. Dani, S. Turillazzi, and J. J. Boomsma. 2007. Chemical mimicry in an incipient leaf-cutting ant social parasite. Behavioral Ecology and Sociobiology 61:843-851

9. (Rand) A large class of environmental toxin, known collectively as endocrine disruptors, has received much attention in both the popular and primary literature. Chemical pollutants from herbicides and pesticides to plastics and livestock waste have been implicated as sources of estrogenic and antiandrogenic compounds. Results from laboratory experiments suggest that some of these endocrine disruptors do not follow classic intercellular and intracellular signaling mechanisms. For example, extremely low doses (well below EPA standards) have been shown to elicit significant reproductive and developmental responses. Thoroughly examine the literature and review a well-studied endocrine system that has been altered by an environmental toxin and that has been studied under controlled laboratory conditions in an attempt to understand the mechanism(s) of disruption.

To get an idea of the wide variety of topics and a list of a few investigators, see:

Colborn, T. 2004 Neurode.velopment and endocrine disruption. Environmental Health Perspectives 112:944-949

10. (Rand) Investigations into the physiological mechanisms regulating appetite have increased due to national concern over rising incidences of eating disorders and obesity. Evidence suggests that circulating and neurosensory signals originating from peripheral structures, such as the stomach and intestines, assist in the regulation of appetite and satiety. Many of these signals either directly or indirectly stimulate orexigenic (eating) or anorexigenic (not eating) circuits within the hypothalamus, which then influence behavioral changes associated with food intake. The peptide hormones, ghrelin, CCK, PYY, insulin, leptin, as well as other signals have been shown to modulate food intake behaviors in a few mammalian model systems. Review the current literature that describes the influence of one or more of these peripheral signals on the hypothalamic pathways that regulate appetite.

Duclos, M., E. Timofeeva, C. Michel, and D. Richard. 2005. Corticosterone-dependent metabolic and neuroendocrine abnormalities in obese Zucker rats in relation to feeding. American Journal of Physiology – Endocrinology and Metabolism 288: E254-E266.

Keen-Rhinehart, E. and T. J. Bartness. 2005. Peripheral ghrelin injections stimulate food intake, foraging, and food hoarding in Siberian hamsters. American Journal of Physiology – Regulatory Integrative and Comparative Physiology 288:R716-R722

Kobelt P., J. J. Tebbe, I. Tjandra, A. Stengel, H. G. Bae, V. Andresen, E. R. van der Voort, R. W. Veh, C. R. Werner, B. F. Klapp, B. Wiedenmann, L. X. Wang, Y. Tache, and H. Monnikes. 2005. CCK inhibits the orexigenic effect of peripheral ghrelin. American Journal of Physiology – Regulatory Integrative and Comparative Physiology 288:R751-R758

Kojima, M. and K. Kangawa. 2005. Ghrelin: structure and function. Physiological Reviews 85:495-522.