2012 AAA Young Investigator Symposium

Below you will find information on our Young Investigator Symposium. To view the details for each listing, please click on the plus (+) sign.

R.R. Bensley Award Lecture in Cell Biology


2012 Award Winner: Jeremy Reiter (Univ. of California, San Francisco)


Tectonics Form a Transition Zone Complex of Ciliopathy Proteins that Regulate Ciliary Composition
Sunday, April 22, 5 - 7 pm

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Primary cilia are projections found on many human cells.  These cilia do not move, but function as cellular antennae to receive and interpret signals.  For example, olfactory cilia sense signals from the environment, such as odorants.  Other cilia sense cues from other cells, such as Hedgehog proteins, to coordinate tissue patterning and growth.  We have identified mechanisms of ciliary signaling, cilium formation, and the regulation of ciliary composition.  Defects in ciliary signaling cause some forms of birth defects, cancer, polycystic kidney disease, and other disorders collectively called ciliopathies.  Investigating ciliopathies is illuminating how disturbing the function of a single organelle can give rise to diverse human diseases.

We have found that two ciliary proteins of the Tectonic family, Tctn1 and Tctn2, form part of the transition zone, a region at the base of the cilium.  Tctn1 is an extracytosolic glycoprotein that interacts with transmembrane components of the transition zone such as Tmem67 to connect to a cytosolic transition zone complex comprised of most known Joubert- and Meckel-associated proteins.  Loss of components of the Tectonic transition zone complex in mice compromise ciliogenesis in some tissues, and deregulate ciliary protein composition in others. We hypothesize that transition zone defects disrupt intercellular signaling, causing the multiorgan disease observed in ciliopathies, including polycystic kidney disease and birth defects such as polydactyly.

Click here for more information on Jeremy Reiter

C.J. Herrick Award Lecture in Comparative Neuroanatomy


2012 Award Winner: Jason Radley (Univ. of Iowa)


Evidence for a Limbic Cortical HPA-inhibitory Network and Its Role in Chronic Stress-induced HPA Axis Hyperactivity
Sunday, April 22, 5 - 7 pm

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A network of interconnected cell groups in the limbic forebrain regulates hypothalamic-pituitary-adrenal (HPA) activation during emotionally stressful experiences, and disruption of these systems is broadly implicated in stress-related psychiatric and systemic illnesses.  A significant challenge to progress has involved unraveling the circuitry and mechanisms providing for regulation of HPA output, as these limbic forebrain regions do provide any direct innervation of HPA effector cell groups in the paraventricular hypothalamus.  While the current view involves a layer of cell groups providing an array multisynaptic parallel pathways between the limbic forebrain and PVH, recent advances in our research will highlight evidence for a discrete region within the bed nucleus of the stria terminalis that serves as a neural hub for receiving and integrating these influences.  Insights gleaned from clarifying the mechanisms of HPA control during acute emotional stress have provided a framework for ongoing studies examining the relationship between chronic stress-induced plasticity in key cell groups (notably, the medial prefrontal cortex) and HPA axis hyperactivity.

Click here for more information on Jason Radley

H.W. Mossman Award Lecture in Developmental Biology


2012 Award Winner: Peter Reddien (Whitehead Institute for Biomedical Research/MIT)


The Cellular and Molecular Basis for Planarian Regeneration
Sunday, April 22, 5 - 7 pm

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The ability to regenerate missing body parts is one of the great mysteries of biology. Planarians are flatworms and a classic regeneration model system. The regenerative abilities of planarians are dramatic: following decapitation, a new head is regenerated in a week and an entire animal can be regenerated from a tiny body fragment. A newly developed arsenal of molecular tools have turned planarians into a powerful molecular genetic system for in vivo investigation of the replacement of missing cells. We determined that there exist pluripotent stem cells, called cNeoblasts, that persist into adulthood and provide the cellular basis for planarian regeneration. We have identified dozens of genes required in vivo for normal cNeoblast physiology. How do wound sites specify what is missing? We investigate the instructions that guide cNeoblasts for the regeneration of appropriate missing structures to understand the molecular basis for regeneration.

Click here for more information on Peter Reddien

AAA Morphological Sciences Award Lecture


2012 Award Winner: Julian Guttman (Simon Fraser Univ.)


Knocking E. coli off of their Pedestals: Understanding the Strategies Microbes Exploit to Generate Morphological Structures during their Disease Processes
Sunday, April 22, 5 - 7 pm

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When the extracellular attaching and effacing pathogens [enteropathogenic E. coli, enterohaemorrhagic E. coli and Citrobacter rodentium] exploit their host cells, morphologically distinct actin-rich structures are generated beneath the attached bacteria. These structures, called pedestals, protrude from the cell surface, enable the bacteria to “surf” atop infected cells and are hallmarks of the infections.  Contained within these structures are numerous actin-associated components that would be predicted to be at dynamic actin-rich structures including the Arp2/3 complex, cortactin, profilin and cofilin. Recently my lab has discovered that unexpected proteins are also present within pedestals. These include clathrin-mediated endocytic proteins and protein components of the spectrin cytoskeleton. These proteins are crucial for pedestal generation as their alteration blocks pedestal formation and often also inhibits attachment of the bacteria to their target cells, thus halting the infections.  By using E. coli pedestals as a model system to also study general cell motility we have shown novel roles for a variety of cellular proteins.  Taken together our examination of E. coli pedestals has already provided potential targets for pharmaceutical intervention as well as novel insights into general cell biological processes.

Click here for more information on Julian Guttman

American Association of Anatomists

9650 Rockville Pike Bethesda, Maryland 20814-3998
Tel: 301-634-7910 | Fax: 301-634-7965

 

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