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DTSTART:20070311T020000
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BEGIN:VEVENT
DTSTAMP:20260408T100351
DTSTART;TZID=America/Detroit:20260413T150000
DTEND;TZID=America/Detroit:20260413T160000
SUMMARY:Workshop / Seminar:MCDB Master's Thesis Defense Seminar> Tissue Maturation and Wound Healing in the Drosophila Prostate-like Accessory Gland
DESCRIPTION:The Drosophila malagonaster (fruit fly) accessory gland (AG) is functionally and structurally analogous to the mammalian prostate and serves as a model for epithelial growth and tissue plasticity. Like the mammalian prostate\, the fly AG consists of two types of  secretory epithelial cells\, an extracellular matrix\, and a surrounding innervated muscle sheath. The secretory epithelium is composed of large\, postmitotic cells that are binucleated and polyploid\, revealing that the differentiation process for the development of this tissue involves extensive cell cycle remodeling\, such as skipping cytokinesis to result in bi-nucleation and skipping M-phases to result in polyploidy. Following eclosion\, the tissue goes through a pronounced growth phase during the first 10 days of adult life. However because this tissue remains post mitotic in the adult\, cell cycle activity during the first 4 hours after adult emergence\, drives growth through a further increase in cell ploidy (chromosome content) during organ maturation. We have also observed that damage to this tissue induces compensatory cellular enlargement through increases in polyploidy\, a response analogous to hypertrophic growth observed in the mammalian liver following a partial hepatectomy. In this study\, RNA sequencing was used to characterize transcriptional dynamics during the first five days post-eclosion to identify gene expression changes underlying early AG growth. In parallel\, tissue wound healing capabilities were assessed using a novel acute puncture model. Recovery following damage was evaluated through fluorescent staining and a damage responsive GFP reporter line\, enabling visualization of cellular responses and identification of candidate pathways in damage induced growth. Together\, these findings provide insight into the molecular mechanisms involved in growth and tissue plasticity in the AG and establish a framework for studying epithelial regeneration in a system that allows for direct genetic analysis.
UID:147150-21900442@events.umich.edu
URL:https://events.umich.edu/event/147150
CLASS:PUBLIC
STATUS:CONFIRMED
CATEGORIES:Biology,Bsbsigns,Thesis Defense
LOCATION:Biological Sciences Building - 1010
CONTACT:
END:VEVENT
BEGIN:VEVENT
DTSTAMP:20260410T172945
DTSTART;TZID=America/Detroit:20260416T120000
DTEND;TZID=America/Detroit:20260416T130000
SUMMARY:Workshop / Seminar:MCDB Master's Thesis Defense Seminar> Calcium and F-actin dynamics  during tricellular zipping in  epithelial junction remodeling
DESCRIPTION:Epithelial cells form adhesive connections through cell-cell junctions\, maintaining a selective barrier despite significant cell shape changes during development and tissue homeostasis. This is accomplished through the active remodeling of cell-cell junctions\, a process largely driven by actomyosin contractility. Using live microscopy of the Xenopus laevis embryonic epithelium\, my lab has characterized “tricellular zipping”\, a vertex remodeling process that contributes to the transition from irregular epithelial cell geometries at the blastula stage to the more regular hexagonal packing that emerges at the gastrula stage of development. Tricellular zipping involves the resolution of a long\, thin cellular extension that stretches toward a vertex where four or more cells meet. As two cells 'zip' together to lengthen a new bicellular interface\, the other cell recedes\, thus forming a new tricellular vertex at the end of zipping. Tricellular zipping is accompanied by transient flashes of cytoplasmic calcium within the long cell extension. My research has focused on investigating these calcium flashes\, whether the calcium flashes are correlated with actomyosin accumulation\, and how pulsatile calcium and actin accumulations drive the elongation of the new bicellular interface between two zipping cells. My data reveals that each tricellular zipping event is accompanied by multiple calcium flashes within the long cellular extension. Following each calcium flash\, there is an increase in the rate of elongation of the new bicellular interface. F-actin also accumulates in a pulsatile fashion within the long cellular extension during tricellular zipping. Cross-correlation analysis demonstrates that calcium flashes are correlated with F-actin accumulation\, and calcium flashes precede F-actin accumulation\, suggesting that pulsatile calcium flashes may activate actin polymerization and/or Myosin II activation during tricellular zipping. Together\, these findings suggest that calcium-associated actomyosin pulses drive tricellular zipping. This research provides new information about an uncharacterized mechanism of junctional remodeling and the emerging role of localized calcium signaling in regulating epithelial junction remodeling during early embryonic development.
UID:147524-21901178@events.umich.edu
URL:https://events.umich.edu/event/147524
CLASS:PUBLIC
STATUS:CONFIRMED
CATEGORIES:Biology,Bsbsigns,Thesis Defense
LOCATION:Biological Sciences Building - 5150
CONTACT:
END:VEVENT
BEGIN:VEVENT
DTSTAMP:20260325T104051
DTSTART;TZID=America/Detroit:20260417T120000
DTEND;TZID=America/Detroit:20260417T130000
SUMMARY:Workshop / Seminar:MCDB Seminar> Tales of algae: from fundamental discovery to application
DESCRIPTION:Although Chlamydomonas is the most well-known “model” organism\, other green algae present interesting physiologies for investigation or offer experimental advantages for research. In addition to the Chlamydomonas genome\, the group has assembled genomes for Dunaliella spp.\, Chromochloris zofingiensis and Auxenochlorella protothecoides. I will present work on the mechanism of translation of nucleus-encoded bicistronic mRNAs\, structural analysis of photosystem I from Fe-deficient Dunaliella spp. and synthetic biology in Auxenochlorella to generate a complex bioproduct. These stories exemplify the contributions to basic and applied research of studies using simple unicellular organisms.\n\nHost: Libo Shan
UID:144932-21896164@events.umich.edu
URL:https://events.umich.edu/event/144932
CLASS:PUBLIC
STATUS:CONFIRMED
CATEGORIES:Biology,Bsbsigns,seminar
LOCATION:Biological Sciences Building - 1060
CONTACT:
END:VEVENT
BEGIN:VEVENT
DTSTAMP:20260408T101640
DTSTART;TZID=America/Detroit:20260421T133000
DTEND;TZID=America/Detroit:20260421T143000
SUMMARY:Workshop / Seminar:MCDB Master's Thesis Defense Seminar> Investing the Role of Cellular Stress on TDP-43 Loss of Function
DESCRIPTION:TDP-43 proteinopathy is a defining hallmark of ALS and FTD. 95% of reported ALS cases result from spontaneous mutations with over 97% being attributed to TDP-43 misfunction. TDP-43 is a nuclear RNA binding protein responsible for RNA metabolism with its most notable role being splicing of RNA. TDP-43 pathology is defined by nuclear clearance known as a loss-of-function and cytoplasmic aggregation\, a gain-of-function. Loss of function results in cryptic splicing leading to the inclusion of cryptic exons that induce frameshifts causing RNA degradation or cryptic peptides. This disruption of cellular homeostasis leads to neuronal death in both cortical and motor neurons\, a defining characteristic of ALS. Studies of the cause of ALS have implicated the exposure to environmental toxins as a risk factor for the progression of ALS. Here we use a fluorescent reporter of TDP-43 cryptic splicing in I3neurons in an assay of 22 environmental toxins to characterize the effects of persistent organic pollutants (POPs) and heavy metals on TDP-43 protein function. We show that increased concentrations of toxins reduce survivability of neurons and increase cryptic splicing events. We conclude that exposure to environmental toxins may contribute to ALS progression by disrupting TDP-43 protein function.
UID:147527-21901180@events.umich.edu
URL:https://events.umich.edu/event/147527
CLASS:PUBLIC
STATUS:CONFIRMED
CATEGORIES:Biology,Bsbsigns,Thesis Defense
LOCATION:Biological Sciences Building - 3150
CONTACT:
END:VEVENT
BEGIN:VEVENT
DTSTAMP:20260327T150419
DTSTART;TZID=America/Detroit:20260423T100000
DTEND;TZID=America/Detroit:20260423T110000
SUMMARY:Workshop / Seminar:MCDB Checkpoint 2 Seminar> Neuroimmune Control of Systemic Shock: The Role of mGluR7 in Shock Propagation
DESCRIPTION:Checkpoint 2 Seminar\nMentor: Gary Huffnagle\, Professor MCDB
UID:147149-21900440@events.umich.edu
URL:https://events.umich.edu/event/147149
CLASS:PUBLIC
STATUS:CONFIRMED
CATEGORIES:Biology,Bsbsigns,Graduate Students
LOCATION:Biological Sciences Building - 1010
CONTACT:
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