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Department of Biology Seminar

"Life by a Thousand Cuts: Archaea as a Model for Evo-Devo Mechanosensing"

Bisson Selfie

Dr. Alex Bisson | Bisson Lab

Abstract:
Cells sense and respond to their physical surroundings, using organized molecular machinery
to convert mechanical environmental signals into biochemical information. Maybe more importantly, little is known about how cells' material properties co-evolve with their
environment. Using genetics, biophysics, and advanced microscopy tools, the Bisson Lab aims to understand archaeal cells' self-organization and behavior in response to physical cues. Here,
I will discuss our recent discovery of how specific mechanical confinement triggers the development from a unicellular to a tissue-like lifestyle similar to known primitive multicellular eukaryotes. This observation not only gives a new perspective over the emergence of complex multicellularity, but gives us the opportunity to compare the behavior and the genome of hundreds of cultivable archaeal species.

Bisson Graphic

Date:
Location:
THM 116

"Life by a Thousand Cuts: Archaea as a Model for Evo-Devo Mechanosensing"

Bisson Selfie

Dr. Alex Bisson | Bisson Lab

Abstract:
Cells sense and respond to their physical surroundings, using organized molecular machinery
to convert mechanical environmental signals into biochemical information. Maybe more importantly, little is known about how cells' material properties co-evolve with their
environment. Using genetics, biophysics, and advanced microscopy tools, the Bisson Lab aims to understand archaeal cells' self-organization and behavior in response to physical cues. Here,
I will discuss our recent discovery of how specific mechanical confinement triggers the development from a unicellular to a tissue-like lifestyle similar to known primitive multicellular eukaryotes. This observation not only gives a new perspective over the emergence of complex multicellularity, but gives us the opportunity to compare the behavior and the genome of hundreds of cultivable archaeal species.

Bisson Graphic

Date:
Location:
THM 116

"Life by a Thousand Cuts: Archaea as a Model for Evo-Devo Mechanosensing"

Bisson Selfie

Dr. Alex Bisson | Bisson Lab

Abstract:
Cells sense and respond to their physical surroundings, using organized molecular machinery
to convert mechanical environmental signals into biochemical information. Maybe more importantly, little is known about how cells' material properties co-evolve with their
environment. Using genetics, biophysics, and advanced microscopy tools, the Bisson Lab aims to understand archaeal cells' self-organization and behavior in response to physical cues. Here,
I will discuss our recent discovery of how specific mechanical confinement triggers the development from a unicellular to a tissue-like lifestyle similar to known primitive multicellular eukaryotes. This observation not only gives a new perspective over the emergence of complex multicellularity, but gives us the opportunity to compare the behavior and the genome of hundreds of cultivable archaeal species.

Bisson Graphic

Date:
Location:
THM 116

"Life by a Thousand Cuts: Archaea as a Model for Evo-Devo Mechanosensing"

Bisson Selfie

Dr. Alex Bisson | Bisson Lab

Abstract:
Cells sense and respond to their physical surroundings, using organized molecular machinery
to convert mechanical environmental signals into biochemical information. Maybe more importantly, little is known about how cells' material properties co-evolve with their
environment. Using genetics, biophysics, and advanced microscopy tools, the Bisson Lab aims to understand archaeal cells' self-organization and behavior in response to physical cues. Here,
I will discuss our recent discovery of how specific mechanical confinement triggers the development from a unicellular to a tissue-like lifestyle similar to known primitive multicellular eukaryotes. This observation not only gives a new perspective over the emergence of complex multicellularity, but gives us the opportunity to compare the behavior and the genome of hundreds of cultivable archaeal species.

Bisson Graphic

Date:
Location:
THM 116

"The Role of Oxytocin Signaling Pathways in the Neuroimmune Response to Mate Bond Dissolution"

Glasper Selfie

Dr. Erica Glasper

Bio:
Erica R. Glasper graduated with honors from Randolph-Macon College in Ashland, Virginia, in 2002 with a major in Psychology and a minor in Biology. Initially pre-med, Erica discovered neuroscience during her freshman year at Randolph-Macon and was selected three times as a Summer Undergraduate Research Fellow. Her research experiences, aided by keen faculty mentorship, set her professional journey in motion. Erica went on to earn an M.A. and Ph.D. in Psychobiology and Behavioral Neuroscience from The Ohio State University. During her time as a postdoctoral scholar at Princeton University, she was supported by a fellowship from the UNCF/Merck Science Initiative and the National Institute on Aging at the National Institutes of Health. In 2011, Dr. Glasper joined the faculty at the University of Maryland – College Park, in the Department of Psychology, as an Assistant Professor. Her research in behavioral neuroendocrinology takes a multidisciplinary approach to understanding how experiences can shape our brains and resulting behavior. Following success as a researcher and educator, she was awarded tenure and promoted to the rank of Associate Professor. During the summer of 2021, the Glasper Lab returned to The Ohio State University, where she joined the Department of Neuroscience and the Institute for Behavioral Medicine Research within the College of Medicine as a tenured Associate Professor. She is excited about continued research success, and her return to the Buckeye State, using a combination of behavioral paradigms along with neuroendocrine, neuroanatomical, neuroimmune, neurochemical, and pharmacological techniques in three lines of research: 1) neurobiology of parenting, 2) neuroprotective role of rewarding social experiences, and 3) enduring consequences of paternal deprivation. Her research is currently funded by the NIH and The Ohio State University Wexner Medical Center.

Abstract:
Loss of a mate results in diverse impairments in bodily and psychological health. In this study, we tested the hypothesis that disrupting a mate bond, in the monogamous California mouse (Peromyscus californicus), would increase the neuroimmune response to a peripheral inflammatory stimulus (lipopolysaccharide [LPS]) through alterations in the oxytocin system. Adult (6-8 months old) male and female mice were exposed to three experimental conditions: 1) single housed, 2) mate bonded, or 3) mate-bonded separation. Mice were either injected with a vehicle (VEH) or an intraperitoneal injection of LPS (1mg/kg) and sacrificed 4-6 hours later.  While mate bond disruption did not increase anxiety-like behavior during open-field testing, physiological indices of mate bond disruption were observed. Males lost significantly more body weight following mate-bond separation, compared to the mate-bonded groups – this effect was not observed in females. Pro-inflammatory cytokine concentration (TNF and IL-1 beta) mRNA levels, measured by RT-qPCR in the hippocampus (HIPP) and hypothalamus (HYPO), were significantly enhanced in LPS-treated female mice following mate bond disruption, compared to the mate-bonded group. Mate bond dissolution did not exacerbate the LPS-induced increase in pro-inflammatory cytokines in males. Disruptions in oxytocin (OXT) signaling may contribute to the increased pro-inflammatory response in LPS-injected mice following mate bond dissolution, as HIPP mRNA levels for the oxytocin receptor (OXTR) in separated males and females were significantly decreased. Independent of endotoxic challenge, TNF and OXTR mRNA levels in separated mice were negatively correlated (as OXTR expression went down, TNF expression went up). Together, these results suggest that the effects of mate bond disruption in neuroimmune responsivity may involve alterations to OXT signaling. 

Watch the seminar here!

Date:
Location:
THM 116

"The Role of Oxytocin Signaling Pathways in the Neuroimmune Response to Mate Bond Dissolution"

Glasper Selfie

Dr. Erica Glasper

Bio:
Erica R. Glasper graduated with honors from Randolph-Macon College in Ashland, Virginia, in 2002 with a major in Psychology and a minor in Biology. Initially pre-med, Erica discovered neuroscience during her freshman year at Randolph-Macon and was selected three times as a Summer Undergraduate Research Fellow. Her research experiences, aided by keen faculty mentorship, set her professional journey in motion. Erica went on to earn an M.A. and Ph.D. in Psychobiology and Behavioral Neuroscience from The Ohio State University. During her time as a postdoctoral scholar at Princeton University, she was supported by a fellowship from the UNCF/Merck Science Initiative and the National Institute on Aging at the National Institutes of Health. In 2011, Dr. Glasper joined the faculty at the University of Maryland – College Park, in the Department of Psychology, as an Assistant Professor. Her research in behavioral neuroendocrinology takes a multidisciplinary approach to understanding how experiences can shape our brains and resulting behavior. Following success as a researcher and educator, she was awarded tenure and promoted to the rank of Associate Professor. During the summer of 2021, the Glasper Lab returned to The Ohio State University, where she joined the Department of Neuroscience and the Institute for Behavioral Medicine Research within the College of Medicine as a tenured Associate Professor. She is excited about continued research success, and her return to the Buckeye State, using a combination of behavioral paradigms along with neuroendocrine, neuroanatomical, neuroimmune, neurochemical, and pharmacological techniques in three lines of research: 1) neurobiology of parenting, 2) neuroprotective role of rewarding social experiences, and 3) enduring consequences of paternal deprivation. Her research is currently funded by the NIH and The Ohio State University Wexner Medical Center.

Abstract:
Loss of a mate results in diverse impairments in bodily and psychological health. In this study, we tested the hypothesis that disrupting a mate bond, in the monogamous California mouse (Peromyscus californicus), would increase the neuroimmune response to a peripheral inflammatory stimulus (lipopolysaccharide [LPS]) through alterations in the oxytocin system. Adult (6-8 months old) male and female mice were exposed to three experimental conditions: 1) single housed, 2) mate bonded, or 3) mate-bonded separation. Mice were either injected with a vehicle (VEH) or an intraperitoneal injection of LPS (1mg/kg) and sacrificed 4-6 hours later.  While mate bond disruption did not increase anxiety-like behavior during open-field testing, physiological indices of mate bond disruption were observed. Males lost significantly more body weight following mate-bond separation, compared to the mate-bonded groups – this effect was not observed in females. Pro-inflammatory cytokine concentration (TNF and IL-1 beta) mRNA levels, measured by RT-qPCR in the hippocampus (HIPP) and hypothalamus (HYPO), were significantly enhanced in LPS-treated female mice following mate bond disruption, compared to the mate-bonded group. Mate bond dissolution did not exacerbate the LPS-induced increase in pro-inflammatory cytokines in males. Disruptions in oxytocin (OXT) signaling may contribute to the increased pro-inflammatory response in LPS-injected mice following mate bond dissolution, as HIPP mRNA levels for the oxytocin receptor (OXTR) in separated males and females were significantly decreased. Independent of endotoxic challenge, TNF and OXTR mRNA levels in separated mice were negatively correlated (as OXTR expression went down, TNF expression went up). Together, these results suggest that the effects of mate bond disruption in neuroimmune responsivity may involve alterations to OXT signaling. 

Watch the seminar here!

Date:
Location:
THM 116

"The Role of Oxytocin Signaling Pathways in the Neuroimmune Response to Mate Bond Dissolution"

Glasper Selfie

Dr. Erica Glasper

Bio:
Erica R. Glasper graduated with honors from Randolph-Macon College in Ashland, Virginia, in 2002 with a major in Psychology and a minor in Biology. Initially pre-med, Erica discovered neuroscience during her freshman year at Randolph-Macon and was selected three times as a Summer Undergraduate Research Fellow. Her research experiences, aided by keen faculty mentorship, set her professional journey in motion. Erica went on to earn an M.A. and Ph.D. in Psychobiology and Behavioral Neuroscience from The Ohio State University. During her time as a postdoctoral scholar at Princeton University, she was supported by a fellowship from the UNCF/Merck Science Initiative and the National Institute on Aging at the National Institutes of Health. In 2011, Dr. Glasper joined the faculty at the University of Maryland – College Park, in the Department of Psychology, as an Assistant Professor. Her research in behavioral neuroendocrinology takes a multidisciplinary approach to understanding how experiences can shape our brains and resulting behavior. Following success as a researcher and educator, she was awarded tenure and promoted to the rank of Associate Professor. During the summer of 2021, the Glasper Lab returned to The Ohio State University, where she joined the Department of Neuroscience and the Institute for Behavioral Medicine Research within the College of Medicine as a tenured Associate Professor. She is excited about continued research success, and her return to the Buckeye State, using a combination of behavioral paradigms along with neuroendocrine, neuroanatomical, neuroimmune, neurochemical, and pharmacological techniques in three lines of research: 1) neurobiology of parenting, 2) neuroprotective role of rewarding social experiences, and 3) enduring consequences of paternal deprivation. Her research is currently funded by the NIH and The Ohio State University Wexner Medical Center.

Abstract:
Loss of a mate results in diverse impairments in bodily and psychological health. In this study, we tested the hypothesis that disrupting a mate bond, in the monogamous California mouse (Peromyscus californicus), would increase the neuroimmune response to a peripheral inflammatory stimulus (lipopolysaccharide [LPS]) through alterations in the oxytocin system. Adult (6-8 months old) male and female mice were exposed to three experimental conditions: 1) single housed, 2) mate bonded, or 3) mate-bonded separation. Mice were either injected with a vehicle (VEH) or an intraperitoneal injection of LPS (1mg/kg) and sacrificed 4-6 hours later.  While mate bond disruption did not increase anxiety-like behavior during open-field testing, physiological indices of mate bond disruption were observed. Males lost significantly more body weight following mate-bond separation, compared to the mate-bonded groups – this effect was not observed in females. Pro-inflammatory cytokine concentration (TNF and IL-1 beta) mRNA levels, measured by RT-qPCR in the hippocampus (HIPP) and hypothalamus (HYPO), were significantly enhanced in LPS-treated female mice following mate bond disruption, compared to the mate-bonded group. Mate bond dissolution did not exacerbate the LPS-induced increase in pro-inflammatory cytokines in males. Disruptions in oxytocin (OXT) signaling may contribute to the increased pro-inflammatory response in LPS-injected mice following mate bond dissolution, as HIPP mRNA levels for the oxytocin receptor (OXTR) in separated males and females were significantly decreased. Independent of endotoxic challenge, TNF and OXTR mRNA levels in separated mice were negatively correlated (as OXTR expression went down, TNF expression went up). Together, these results suggest that the effects of mate bond disruption in neuroimmune responsivity may involve alterations to OXT signaling. 

Watch the seminar here!

Date:
Location:
THM 116

"The Role of Oxytocin Signaling Pathways in the Neuroimmune Response to Mate Bond Dissolution"

Glasper Selfie

Dr. Erica Glasper

Bio:
Erica R. Glasper graduated with honors from Randolph-Macon College in Ashland, Virginia, in 2002 with a major in Psychology and a minor in Biology. Initially pre-med, Erica discovered neuroscience during her freshman year at Randolph-Macon and was selected three times as a Summer Undergraduate Research Fellow. Her research experiences, aided by keen faculty mentorship, set her professional journey in motion. Erica went on to earn an M.A. and Ph.D. in Psychobiology and Behavioral Neuroscience from The Ohio State University. During her time as a postdoctoral scholar at Princeton University, she was supported by a fellowship from the UNCF/Merck Science Initiative and the National Institute on Aging at the National Institutes of Health. In 2011, Dr. Glasper joined the faculty at the University of Maryland – College Park, in the Department of Psychology, as an Assistant Professor. Her research in behavioral neuroendocrinology takes a multidisciplinary approach to understanding how experiences can shape our brains and resulting behavior. Following success as a researcher and educator, she was awarded tenure and promoted to the rank of Associate Professor. During the summer of 2021, the Glasper Lab returned to The Ohio State University, where she joined the Department of Neuroscience and the Institute for Behavioral Medicine Research within the College of Medicine as a tenured Associate Professor. She is excited about continued research success, and her return to the Buckeye State, using a combination of behavioral paradigms along with neuroendocrine, neuroanatomical, neuroimmune, neurochemical, and pharmacological techniques in three lines of research: 1) neurobiology of parenting, 2) neuroprotective role of rewarding social experiences, and 3) enduring consequences of paternal deprivation. Her research is currently funded by the NIH and The Ohio State University Wexner Medical Center.

Abstract:
Loss of a mate results in diverse impairments in bodily and psychological health. In this study, we tested the hypothesis that disrupting a mate bond, in the monogamous California mouse (Peromyscus californicus), would increase the neuroimmune response to a peripheral inflammatory stimulus (lipopolysaccharide [LPS]) through alterations in the oxytocin system. Adult (6-8 months old) male and female mice were exposed to three experimental conditions: 1) single housed, 2) mate bonded, or 3) mate-bonded separation. Mice were either injected with a vehicle (VEH) or an intraperitoneal injection of LPS (1mg/kg) and sacrificed 4-6 hours later.  While mate bond disruption did not increase anxiety-like behavior during open-field testing, physiological indices of mate bond disruption were observed. Males lost significantly more body weight following mate-bond separation, compared to the mate-bonded groups – this effect was not observed in females. Pro-inflammatory cytokine concentration (TNF and IL-1 beta) mRNA levels, measured by RT-qPCR in the hippocampus (HIPP) and hypothalamus (HYPO), were significantly enhanced in LPS-treated female mice following mate bond disruption, compared to the mate-bonded group. Mate bond dissolution did not exacerbate the LPS-induced increase in pro-inflammatory cytokines in males. Disruptions in oxytocin (OXT) signaling may contribute to the increased pro-inflammatory response in LPS-injected mice following mate bond dissolution, as HIPP mRNA levels for the oxytocin receptor (OXTR) in separated males and females were significantly decreased. Independent of endotoxic challenge, TNF and OXTR mRNA levels in separated mice were negatively correlated (as OXTR expression went down, TNF expression went up). Together, these results suggest that the effects of mate bond disruption in neuroimmune responsivity may involve alterations to OXT signaling. 

Watch the seminar here!

Date:
Location:
THM 116

"The Role of Oxytocin Signaling Pathways in the Neuroimmune Response to Mate Bond Dissolution"

Glasper Selfie

Dr. Erica Glasper

Bio:
Erica R. Glasper graduated with honors from Randolph-Macon College in Ashland, Virginia, in 2002 with a major in Psychology and a minor in Biology. Initially pre-med, Erica discovered neuroscience during her freshman year at Randolph-Macon and was selected three times as a Summer Undergraduate Research Fellow. Her research experiences, aided by keen faculty mentorship, set her professional journey in motion. Erica went on to earn an M.A. and Ph.D. in Psychobiology and Behavioral Neuroscience from The Ohio State University. During her time as a postdoctoral scholar at Princeton University, she was supported by a fellowship from the UNCF/Merck Science Initiative and the National Institute on Aging at the National Institutes of Health. In 2011, Dr. Glasper joined the faculty at the University of Maryland – College Park, in the Department of Psychology, as an Assistant Professor. Her research in behavioral neuroendocrinology takes a multidisciplinary approach to understanding how experiences can shape our brains and resulting behavior. Following success as a researcher and educator, she was awarded tenure and promoted to the rank of Associate Professor. During the summer of 2021, the Glasper Lab returned to The Ohio State University, where she joined the Department of Neuroscience and the Institute for Behavioral Medicine Research within the College of Medicine as a tenured Associate Professor. She is excited about continued research success, and her return to the Buckeye State, using a combination of behavioral paradigms along with neuroendocrine, neuroanatomical, neuroimmune, neurochemical, and pharmacological techniques in three lines of research: 1) neurobiology of parenting, 2) neuroprotective role of rewarding social experiences, and 3) enduring consequences of paternal deprivation. Her research is currently funded by the NIH and The Ohio State University Wexner Medical Center.

Abstract:
Loss of a mate results in diverse impairments in bodily and psychological health. In this study, we tested the hypothesis that disrupting a mate bond, in the monogamous California mouse (Peromyscus californicus), would increase the neuroimmune response to a peripheral inflammatory stimulus (lipopolysaccharide [LPS]) through alterations in the oxytocin system. Adult (6-8 months old) male and female mice were exposed to three experimental conditions: 1) single housed, 2) mate bonded, or 3) mate-bonded separation. Mice were either injected with a vehicle (VEH) or an intraperitoneal injection of LPS (1mg/kg) and sacrificed 4-6 hours later.  While mate bond disruption did not increase anxiety-like behavior during open-field testing, physiological indices of mate bond disruption were observed. Males lost significantly more body weight following mate-bond separation, compared to the mate-bonded groups – this effect was not observed in females. Pro-inflammatory cytokine concentration (TNF and IL-1 beta) mRNA levels, measured by RT-qPCR in the hippocampus (HIPP) and hypothalamus (HYPO), were significantly enhanced in LPS-treated female mice following mate bond disruption, compared to the mate-bonded group. Mate bond dissolution did not exacerbate the LPS-induced increase in pro-inflammatory cytokines in males. Disruptions in oxytocin (OXT) signaling may contribute to the increased pro-inflammatory response in LPS-injected mice following mate bond dissolution, as HIPP mRNA levels for the oxytocin receptor (OXTR) in separated males and females were significantly decreased. Independent of endotoxic challenge, TNF and OXTR mRNA levels in separated mice were negatively correlated (as OXTR expression went down, TNF expression went up). Together, these results suggest that the effects of mate bond disruption in neuroimmune responsivity may involve alterations to OXT signaling. 

Watch the seminar here!

Date:
Location:
THM 116

"The Problem of Time in Climate Change Ecology"

Wolkovich Selfie

Dr. Elizabeth Wolkovich | Wolkovich Lab

Bio
Elizabeth Wolkovich is an Associate Professor in Forest and
Conservation Sciences and Canada Research Chair at the University of British Columbia. She runs the Temporal Ecology Lab, which focuses on understanding how climate change shapes plants and plant communities, with a focus on shifts in the timing of seasonal development (e.g., budburst, flowering and fruit maturity)---known as phenology. Her lab both collects new data on forest trees and winegrapes and collates existing data to provide global estimates of shifts in phenology with warming from plants to birds and other animals, and to understand how human choices will impact future winegrowing regions. Her research benefits from an interdisciplinary team of collaborators from agriculture, biodiversity science, climatology, evolution and viticulture, as well as from shared long-term datasets from across North America and Europe.

Abstract
Forty years ago ecology became increasingly focused on spatial structure and pattern, as researchers realized how fundamentally habitat loss and fragmentation reshapes populations and communities. A generation later, with spatial ecology firmly established as a cross-disciplinary, multi-scale field, anthropogenic climate change has forced ecology to revisit the importance of time. As warming stretches growing seasons around the globe, populations, species, communities and ecosystems are responding in turn. In this talk I outline two major challenges of temporal ecology with anthropogenic warming: stretched time and accelerated time. Focusing on
plant phenology I show how longer growing seasons may re-assemble communities: first I focus on examples from invasion biology then I build to a more general theory. Next I show how how warming may make many biological processes that are dependent on thresholds appear to slow as warming continues. This is because warming accelerates biological time while calendar time stands still. I close by reviewing preliminary results that merge phenological cues with trait ecology to show that forests may assemble via their spring phenology.

Watch the seminar here

Date:
Location:
THM 116