All colloquia are in TBL 112 at 1:10pm on the dates below (except where noted).
September 19, 20 (BIMO 60s Scholar): Dr. Rick Morimoto, Northwestern University
“Proteostasis – Protecting the Proteome in Biology, Aging, and Disease”
Understanding the principles underlying CELLULAR QUALITY CONTROL — the integration of processes by which the cell senses, responds and adapts to environmental and physiological challenges — is among the most fascinating problems in biology. The appearance of incorrectly expressed or improperly folded proteins results in a cellular stress response involving activation of stress-induced transcription factors and leads to the elevated expression of molecular chaperones and proteases that serve to clear damaged proteins. An imbalance in protein homeostasis results in the accumulation of misfolded and aggregation-prone proteins that are poorly refolded and degraded, often accumulating as oligomeric intermediate species and aggregates in different subcellular compartments. These events are hallmarks of human genetic diseases including the polyglutamine-expansion diseases such as Huntington’s disease, Parkinson’s disease, Alzheimer’s disease, familial ALS, prion diseases, amyloidosis, cystic fibrosis, and a-1-antitrypsin disease. Our laboratory is interested in the fundamental events that underlie the appearance of misfolded proteins and their consequence to protein homeostasis, cellular function, and organismal adaptation and survival.
September 27: Dr. Jesse Bellemare, Smith College
“Climate Change and Plant Conservation in the Forests of Eastern North America”
Climate change will be a top threat to biodiversity in coming decades. Species with small ranges, i.e. endemics, may be at increased risk of extinction, as unsuitable conditions may develop rapidly across the entirety of their ranges. Human-assisted colonization or “managed relocation” has been proposed as one option to avoid extinctions by facilitating species in tracking suitable conditions poleward. In this research we conducted a biogeographic GIS analysis to document where small-ranged endemic species are concentrated in the forests of eastern North America and how these distribution and diversity patterns might relate to past climate change and the threats posed by modern, anthropogenic climate change. We found that endemic forest plants are highly concentrated in the Southeast US, but largely absent from areas near and north of the boundary of the last glacial maximum in the Northeast and upper Midwest. The patterns detected suggest that many small-ranged species’ distributions are still impacted by past climate change and that they might be slow to respond to modern challenges. In parallel to the GIS study, we also launched an on-the-ground experiment testing the feasibility of northward managed relocation with one of the small-ranged endemics investigated in the biogeographic analysis, Umbrella-leaf (Diphylleia cymosa, Berberidaceae). This forest herb is endemic to high elevation forests in the southern Appalachian Mountains of western North Carolina. In Fall 2008, we established a ~1000 km transect of seed sowing sites from 3 locations within the species’ native range to 5 apparently suitable, but unoccupied, sites outside the range in the Mid-Atlantic and Northeast US. Germination in 2009 was relatively high overall (44%) and did not differ significantly within vs. beyond the species’ range (40% vs. 46%). Survival from the seedling to juvenile stage (2009-2010) was significantly higher inside vs. outside the range (63% vs. 30%), possibly due to increased herbivory beyond the native range. However, 2010-13 survival rates have been comparable inside vs. outside the range as juveniles have become established. Growth rates of experimental plants outside the native range have been higher than those within the range, despite increased herbivory, and sexual reproduction is possible in 2014. Overall, these results suggest that the distributions of many small-ranged forest plants may still be recovering from past climate change and that assisted colonization could be an option for some endemic species threatened by modern climate change.
October 4, 11, 18: Mountain Day / Thesis Talks
October 24, 25 (Class of 60s Scholar): Dr. Rebecca Nelson, Cornell Univeristy
“Understanding disease resistance in maize: genetic architecture, QTL and pleiotropic effects”
It is important to protect crops from the many pathogens that attack them. Breeding resistant varieties is probably the most effective single approach to disease management. The Nelson lab works on the genetic analysis of disease resistance in maize, with the aim of contributing to sustainable disease management. Many loci in the maize genome have been identified that contribute to reducing disease severity. We have proposed that quantitative disease resistance is based on diverse mechanisms, presumably involving genes involved in avoidance, perception, signaling and response. Because genes involved in development, morphology, signaling and defense may entail physiological costs and trade-offs, this raises the possibility that disease resistance is associated with other, potentially undesirable, traits. Pleiotropic effects of interest would include those resistant traits that affect crop yields; those cases in which resistance to one disease is associated with resistance or susceptibility to another; and cases in which resistance is associated with a phenotype that sheds light on the underlying mechanism of resistance. Recent findings pertaining to the issue of multiple disease resistance and pleiotropy with respect to quantitative resistance to maize will be presented. Evidence includes correlation analyses in segregating populations, fine mapping of selected QTL, association mapping for multiple traits, and analysis of mutants at candidate gene loci.
November 1: Dr. Jennifer Morgan, Marine Biological Laboratory
“Roles for Synuclein in Spinal Cord Injury and Parkinson’s Disease”
Spinal cord injury causes widespread death of neurons, thereby limiting regeneration and recovery. At present, little is known about how to improve the survival of damaged neurons after injury. To address this, our lab is taking advantage of the giant reticulospinal (RS) neurons in sea lampreys (Petromyzon marinus), which permit an examination of post-injury cellular and molecular responses at the level of individual neurons. In lampreys, some of the identified giant RS neurons reproducibly die after injury, while others survive the injury. By studying the molecular responses in these cells, we can identify specific molecular factors that govern cell death or survival after injury, which is difficult – if not impossible – in other vertebrate experimental models. We recently discovered some interesting parallels between neurodegeneration in spinal cord injury and that observed in Parkinson’s Disease. Specifically, we observed cell-specific accumulation of the neuronal protein, synuclein, into neurotoxic aggregates only in the subset of neurons that degenerate after injury. Using imaging and knockdown approaches, we have further shown that reducing the accumulation of synuclein consequently increases neuronal survival and improves axon sprouting and regeneration after spinal cord injury. Thus, synuclein accumulation is a risk factor for neurodegeneration after injury, as it is in Parkinson’s Disease, suggesting that this process may be a new therapeutic target for improving recovery from spinal cord injury.
November 8: Dr. Stephen DiCarlo, Wayne State University
“Sympathetic Neuroplasticity Following T5 Spinal Cord Transection Increases the Susceptibility to Ischemia-induced Sustained Ventricular Tachycardia”
Spinal cord injury-induced neuroplasticity within sympathetic pathways causes cardiac dysfunction and increases the susceptibility to life-threatening ventricular arrhythmias. For example, using coronary artery occlusion, we documented a dramatic increase in the susceptibility to ventricular tachy-arrhythmias in conscious rats with mid-thoracic spinal cord injury (T5X). Furthermore, using injections of cholera toxin B into the left and right stellate ganglia, as well as pericardial sac, and using the Sholl analyses, we documented that stellate-projecting sympathetic pre-ganglionic neurons within spinal segments T1-T5 as well as cardiac projecting sympathetic post-ganglionic neurons within the stellate ganglia from T5X rats have larger dendritic trees than uninjured rats. The hearts of rats with T5X are also hyper-innervated by tyrosine hydroxylase (TH)-immunoreactive sympathetic axons. These neuroplastic changes are associated with an increased nerve growth factor content within the heart and stellate ganglia. Thus, by using a combination of techniques and lines of evidence, we documented that mid-thoracic spinal cord injury results in cardiac sympathetic hyper-innervation and increased susceptibility to life-threatening ventricular arrhythmias. These results have important implications for understanding the mechanisms responsible for the high mortality rates and incidence of cardiovascular disease in individuals with spinal cord injury.
February 7: Magdalena Bezanilla, University of Massachusetts
February 14: Winter Carnival
February 21: BIMO Reunion
February 27, 28 (Class of 60s Scholar): Elissa Hallem ’99, UCLA
March 7 (BIMO Class of 60s Scholar): Mike Snyder, Stanford University
March 14: Hadley Horch, Bowdoin
April 11: Melina Hale, University of Chicago
April 18: Ajay Dhaka, University of Washington, Seattle
April 25: Claire Ting, Sigma Xi Talk
May 2: Thesis Poster Presentations, TBL Lobby 1:00 – 3:00
Previous Years Schedule