Natalie Saini, Ph.D.
National Institute of Environmental Health Sciences

ABSTRACT
Accumulation of somatic mutations over the lifetime of an individual can be facilitated by genetic factors like impaired DNA repair pathways, and by exogenous DNA damaging agents.  The large-scale cancer genome sequencing projects have demonstrated that mutation load and spectra in cancer genomes are characteristic of the cell and type tissue, location in the body, and environmental exposures.  However, accurate measurements of lifetime accumulation of genetic changes attributable to these factors in healthy human cells are lacking.  Previously, we demonstrated that mutation loads and spectra in the genomes of single skin fibroblast-derived clonal lineages from two healthy individuals resemble cancers.  We showed that while, all samples carry CàT changes at CpG dinucleotides (the aging-associated mutation signature), cells from sun-exposed body sites carry a higher mutation burden with a predominant UV–induced mutation signature as compared to unexposed sites.  Somatic mutation load also can be used as a measure of the ability of the cells to repair lesions.  As such, we hypothesize that individuals with potentially deleterious polymorphisms in DNA repair genes, would have higher mutation loads and different mutational spectra than carriers of functional alleles.  We have obtained DNA from >3000 individuals via the NIEHS Environmental Polymorphisms Registry.  Amplification of potential DNA repair genes with asymmetric barcodes, and sequencing via the Pacific Biosciences single molecule real-time sequencing technology is used for identifying healthy individuals with common and rare deleterious alleles in the given gene.  Sequencing single cell-derived clones from these individuals provides the range of mutation loads, and predominant mutation signatures attributable to defects in DNA repair pathways across a population.

Host: Kirill Lobachev, Ph.D.

A unique treat awaits fans at the Yellow Jackets’ Jan. 22 men’s basketball home game. The Georgia Tech team will battle Notre Dame’s Fighting Irish for the hoops amid element cards, games, and prizes to celebrate 2019, the International Year of the Periodic Table of the Chemical Elements.  

Born 150 years ago, the periodic table is one of the most important and recognizable tools of science. To celebrate the table’s staying power, the United Nations proclaimed 2019 as the International Year of the Periodic Table of Chemical Elements.

At Georgia Tech, the College of Sciences is leading an all-year-round celebration, #IYPT2019GT. It has partnered with other units to engage students, faculty, and staff in reconnecting with the periodic table, through athletics, art, and academics.

Kicking off the celebration is “The Periodic Table at Georgia Tech vs Notre Dame” men’s basketball match on Jan. 22. Partnering with Georgia Tech Athletics, the College of Sciences will bring #IYPT2019GT to McCamish Pavilion. Fans will have a chance to play games with the periodic table and element cards featuring the Yellow Jackets basketball team and Georgia Tech researchers. Prizes await lucky winners.  

Admission is free to Georgia Tech students with a valid BuzzCard.  

Discounted tickets are available to Georgia Tech faculty and staff here. 

Parking for Fans and Visitors

To purchase guaranteed gameday parking in advance ($12 plus service fee), visit the Click and Park website. Cash payments ($15) are also accepted at each parking location listed below (attendants from Standard Parking Plus will be collecting parking fees).

Fans are allowed to park in E40, E52, ER55 (Fowler Street only), E63, E65, ER66 and W23. Click here for more information on parking zones. For weekend games, parking areas open four (4) hours before tipoff. For weekday games, parking areas open at 5:00 p.m.​

Visitors who arrive before these areas open are welcome to park in the GT Hotel and Conference Center parking deck (E81) in Tech Square or in Visitors’ Area 6 at $1.50 per hour.

Please note the following regulations:

• Parking on sidewalks, lawns, green space or landscaped areas is prohibited.
• Vehicles found in violation will be subject to impoundment and fines.

Go Yellow Jackets!

A Frontiers in Science Lecture to celebrate 2019, the International Year of the Periodic Table

The creation of the elements in the universe took billions of years and required various processes.

The first few minutes of the big bang produced only hydrogen (H) and helium (He). No new elements were formed until a few hundred million years later when the first generation of stars were born and they started fusing H and He into slightly higher-mass elements, such as carbon and oxygen. Various fusion reactions by multiple generations of stars eventually created elements up to iron (Fe).

However, normal stars cannot produce elements beyond Fe. Creation of elements heavier than Fe required the cataclysmic explosions of supernovas. These violent deaths of massive stars not only completed the natural elements in the periodic table. They also enabled human life, because certain life processes require heavy elements.

About the Speaker
James “Jim” Sowell is an astronomer at Georgia Tech and the director of the Georgia Tech Observatory. He has taught Georgia Tech’s two Introductory Astronomy courses for 27 years and the advanced Stellar Astrophysics course for 20 years. 

He won the inaugural CETL Undergraduate Educator Award in 2009.  He often performs public outreach and education, including the widely popular, monthly Public Nights at the Observatory; presentations at schools; and workshops for K-12 teachers. He developed the Aloha Telescope. This remotely controlled facility in Hawaii allows Atlanta area K-12 teachers and students to view live images of the Moon during regular school hours. 

Sowell earned B.S. and M.S. degrees from Vanderbilt University and a Ph.D. from the University of Michigan. He joined Georgia Tech in 1989.

About Frontiers in Science Lectures
Lectures in this series are intended to inform, engage, and inspire students, faculty, staff, and the public on developments, breakthroughs, and topics of general interest in the sciences and mathematics. Lecturers tailor their talks for nonexpert audiences.

About the Periodic Table Frontiers in Science Lecture Series
Throughout 2019, the College of Sciences will bring prominent researchers from Georgia Tech and beyond to expound on little-discussed aspects of chemical elements:

• Feb. 6, James Sowell, How the Universe Made the Elements in the Periodic Table
• March 5, Michael Filler, Celebrating Silicon: Its Success, Hidden History, and Next Act
• April 2, John Baez, University of California, Riverside, Mathematical Mysteries of the Periodic Table
• April 18, Sam Kean, Author, The Periodic Table: A Treasure Trove of Passion, Adventure, Betrayal, and Obsession
• Sept. 12, Monica Halka, The Elusive End of the Periodic Table: Why Chase It?
• October, Taka Ito, Turning Sour, Bloated, and Out of Breath: Ocean Chemistry under Global Warming (This will take place on the Thursday of Homecoming Week 2019)
• Nov. 12, Margaret Kosal, The Geopolitics of Rare and Not-So-Rare Elements

Closest public parking is Visitors Area 2, on Ferst Street by the Student Center, http://pts.gatech.edu/visitors#l3  

Refreshments served after every lecture

Han Wang, Ph.D.
Division of Biology and Biological Engineering
California Institute of Technology

ABSTRACT
Sleep is a fundamental process that is essential for survival, but remains one of the most intriguing mysteries in biology. Sleep disorders in humans are prevalent and abnormal sleep can lead to adverse effects on neuronal function and contribute to various diseases. However, it is unclear how sleep is controlled at the molecular and circuit levels. By studying stress-induced sleep in C. elegans, I identified several novel sleep regulators and discovered a new mechanism underlying sleep regulation by neuropeptide signaling. I have also been developing genetic tools for systematic dissection of neural circuits for sleep in C. elegans. Specifically, I engineered a “cool” GAL4 to develop a bipartite cGAL system and its split derivative that allow unprecedented genetic access to the C. elegans nervous system at single neuron resolution. I am currently working on the characterization of novel sleep regulators and using the cGAL system for functional circuit mapping for sleep in C. elegans.

Host: Dr. Annalise Paaby

Hillary Young, Ph.D.
Department of Ecology, Evolution, and Marine Biology
University of California, Santa Barbara

ABSTRACT
While we often think of the decline of wild animal life on our planet as merely a tragic consequence of other forms of global change, this defaunation is in fact a driver of global change in its own right, with cascading effects to ecosystem function. Here, I characterize the current Anthropocene defaunation event and, using a case study on zoonotic disease, explore how defaunation affects ecosystem function.  Specifically I ask how we can understand the variability in these responses across environmental contexts in order to better predict and interrupt the negative functional consequences of this modern pulse of defaunation.

ABOUT THE SPEAKER
Hillary Young is a community ecologist in the department of Ecology, Evolution, and Marine Biology at UC Santa Barbara. Dr. Young received a B.A. degree in Ecology and Evolutionary Biology at Princeton University. She then received an M.A. in Environmental Management at Yale University where she focused on applied forest management questions. Her PhD in Biology at Stanford University examined cascading effects of changes in plant communities on whole ecosystem and community structure. As a postdoctoral researcher jointly affiliated at Smithsonian Institution and Harvard University she examined the impacts of anthropogenic disturbance on mammal communities and ultimately, on zoonotic diseases.

Host: Mark Hay, Ph.D.

Yi Gu, Ph.D.
Princeton Neuroscience Institute
Princeton University

ABSTRACT
The ability of knowing where we are and finding our way during spatial navigation is closely associated with an “inner GPS” in the brain, the hippocampal-entorhinal circuit. The medial entorhinal cortex (MEC) contains “grid cells”, which have one of the most mysterious activity patterns in the brain, as their firing fields lie on a triangular lattice when animals navigate in an open arena. These grid cells together may serve as a coordinate system allowing precise positioning during navigation. Here I will present my study on grid cells in understanding the formation of their activity patterns and their roles in path integration. First, combining cellular-resolution two-photon imaging and virtual reality, I revealed a topographical map of grid cells in the mouse MEC according to their firing properties. This map contributes to a foundation for evaluating circuit models of grid cell network and is consistent with continuous attractor models as the mechanism of grid formation. Second, I discovered a novel cell type, “cue cell”, in the MEC. Cue cells specifically encode landmark information during virtual navigation and are potentially important for correcting errors in grid cell network during path integration. In my future laboratory, I will develop multifaceted research programs to understand the MEC in both health and disease at the circuit and molecular levels.

Nathan Klapoetke, Ph.D.
HHMI
Janelia Research Campus

ABSTRACT
Nervous systems combine lower-level sensory signals to generate higher-order representations for guiding natural and voluntary behaviors. In this talk, I describe my research on how looming is encoded by the visual system to enable flies to identify and escape threats. I will also discuss how the fly visual system is able to compute object shapes and motion in general, and how the underlying neuronal architecture can support a broad range of visually guided natural behaviors.

Shannon Stephens
School of Medicine
University of California, San Diego

ABSTRACT
Reproduction is comprised of many complex behavioral and physiological processes. My research examines how the brain controls reproductive physiology and behavior, focusing on the role of kisspeptin in regulating reproduction. Kisspeptin, encoded by Kiss1, is a potent stimulator of the reproductive axis and humans and mice with mutations in Kiss1 or its receptor, Kiss1r, have severe deficits in puberty onset, gonadal sex steroid hormone production, and fertility. Thus, kisspeptin is required for reproduction. Despite much research, the mechanisms regulating Kiss1 neurons and the reproductive axis have yet to be fully characterized. My early postdoctoral research examined the regulation and function of hypothalamic Kiss1 neurons, demonstrating that progesterone acts directly on kisspeptin neurons to regulate female fertility. My research also showed that treatment with corticosterone, a stress hormone, impaired female fertility and this was likely the result of reduced hypothalamic Kiss1 expression and Kiss1 neuronal activation in corticosterone-treated females. Kiss1 neurons are located primarily within the hypothalamus but are also detected in other brain areas, such as the medial amygdala (MeA). However, virtually nothing is known about the regulation and function of Kiss1 neurons in the MeA, which is the focus of my ongoing and future research. The amygdala is implicated in regulating reproduction, as well numerous other behavioral and physiological events such as stress, anxiety, and social behavior. Understanding the regulation and function of Kiss1 neurons in the MeA may provide valuable insight regarding how the amygdala modulates reproductive hormones and how amygdala-dependent behaviors, such as stress, can alter reproduction.

Zizhen Wu, Ph.D.
Department of Neuroscience
John Hopkins University

ABSTRACT
Auditory hair cells contain mechanotransduction channels that rapidly open in response to sound-induced vibrations. We found that auditory hair cells contain two molecularly distinct mechanotransduction channels. One ion channel is activated by sound and is responsible for sensory transduction. This sensory transduction channel is expressed in hair cell stereocilia, and previous studies show that its activity is affected by mutations in the genes encoding the transmembrane proteins TMHS, TMIE, TMC1 and TMC2. We show here that the second ion channel is expressed at the apical surface of hair cells and that it contains the Piezo2 protein. The activity of the Piezo2-dependent channel is controlled by the intracellular Ca2+ concentration and can be recorded following disruption of the sensory transduction machinery or more generally by disruption of the sensory epithelium. We thus conclude that hair cells express two molecularly and functionally distinct mechanotransduction channels with different subcellular distributions.