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DTSTAMP:20261023T103023
DTSTART;TZID=America/Detroit:20261109T150000
DTEND;TZID=America/Detroit:20261109T160000
SUMMARY:Workshop / Seminar:MCDB Seminar> How Dynein Teams Adapt to Load and Coordinate Their Motors
DESCRIPTION:Cytoplasmic dynein drives long-distance transport along microtubules\, but how motor complexes adapt to mechanical loads and coordinate their activities remains poorly understood. I will present our discovery that the dynein–dynactin–BicD2 (DDB) complex dynamically recruits a third dynein under load through an auxiliary BicD2 adaptor that interacts with the dynein light intermediate chain (LIC)\, increasing force generation from 7 to 9 pN. I will also show how our investigation of the neurodevelopmental disease-associated DYNC1H1 mutation P3018S revealed that the trailing dynein determines the velocity of multi-dynein complexes\, while the leading dynein stimulates the trailing motor through its LIC. Together\, these findings uncover unexpected roles for LICs in load-dependent motor recruitment and inter-motor communication\, establishing new principles of dynein force adaptation and coordination.\n\n\nThe Gennerich Lab investigates the molecular mechanisms by which biomolecular motors generate force and motion in eukaryotic cells. We focus on understanding how defects in these processes contribute to human disease. Our research combines single-molecule biophysics\, molecular biology\, and biochemistry to study the function and regulation of microtubule-based motors—kinesins and cytoplasmic dynein—as well as RNA polymerase II during transcription elongation through chromatin.\n\nUsing a multidisciplinary approach that includes high-resolution optical trapping\, single-molecule fluorescence microscopy\, and CRISPR-Cas9-based genetic tools\, we dissect how these motor proteins convert chemical energy into mechanical work and how their activity is modulated in different cellular contexts. Our long-term goal is to uncover the design principles of biomolecular motors and to elucidate the molecular basis of diseases caused by impaired motor function.
UID:154033-21917057@events.umich.edu
URL:https://events.umich.edu/event/154033
CLASS:PUBLIC
STATUS:CONFIRMED
CATEGORIES:Biology,Bsbsigns
LOCATION:Biological Sciences Building - 1010
CONTACT:
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BEGIN:VEVENT
DTSTAMP:20261027T103923
DTSTART;TZID=America/Detroit:20261120T120000
DTEND;TZID=America/Detroit:20261120T130000
SUMMARY:Workshop / Seminar:MCDB Seminar Series> Refuse to choose:  Leveraging preclinical cancer models for basic discovery
DESCRIPTION:Abstract: Professor Mcclatchey will share her lab’s efforts to develop in vivo and 3D models of glial and epithelial tumors\, and to deploy them for both preclinical and mechanistic studies. Their studies have uncovered unexpected ways in which cellular states impact morphogenesis\, oncogene signaling and drug response\, highlighting the value of this approach.\n\nBio: The McClatchey laboratory seeks to understand how cells organize their outer membrane or cortex\, which\, in turn\, determines their identity\, behavior\, and interface with the external environment. Cancer cells exhibit defective membrane organization and therefore interact inappropriately with other cells and with their environment.\n\nOur research stems from a longstanding dedication to understanding the molecular basis of neurofibromatosis type 2 (NF2)\, a familial tumor syndrome caused by mutation of the NF2 tumor suppressor gene. The NF2-encoded protein\, Merlin\, and closely related ERM proteins (Ezrin\, Radixin\, and Moesin) are key architects of the cell cortex.
UID:151241-21911139@events.umich.edu
URL:https://events.umich.edu/event/151241
CLASS:PUBLIC
STATUS:CONFIRMED
CATEGORIES:Biology,Bsbsigns
LOCATION:Biological Sciences Building - 1060
CONTACT:
END:VEVENT
BEGIN:VEVENT
DTSTAMP:20261026T135306
DTSTART;TZID=America/Detroit:20261204T120000
DTEND;TZID=America/Detroit:20261204T130000
SUMMARY:Workshop / Seminar:MCDB Seminar Series> The impact of genetic cheating on mammalian reproduction and speciation
DESCRIPTION:Abstract: Genetic elements compete for transmission to the next generation through meiosis\, when haploid gametes are created from a diploid parent. Although Mendel's Law of Segregation states that each genetic element has an equal chance to transmit to the gametes\, it is becoming increasingly clear that this law is often violated by selfish elements. This non-Mendelian transmission of selfish elements in meiosis is called meiotic drive with significant impacts on chromosome evolution and fertility. I will present two unpublished stories on meiotic drive and its impact on speciation\, both of which take advantage of rich natural variations and species divergence in mouse species.\n\nBio: Dr. Takashi Akera graduated from the University of Tokyo with a Ph.D. in Biophysics and Biochemistry in 2014. He conducted postdoctoral research at the University of Pennsylvania in the laboratory of Dr. Michael Lampson from 2015 to 2019. He received both Holtzer Award for outstanding postdoctoral research in Cell and Developmental Biology and Kaushal Award for excellence in postdoctoral research in Genetics from the University of Pennsylvania in 2018. Dr. Akera joined the NHLBI in 2019 as an Earl Stadtman tenure-track Investigator and has made fundamental advances in the understanding of genetic cheating and its impact on mammalian reproduction and speciation. He has received the 2024 NHLBI Outstanding Mentor Award and the 2026 Vilcek Prize for Creative Promise in Biomedical Sciences.
UID:151242-21911140@events.umich.edu
URL:https://events.umich.edu/event/151242
CLASS:PUBLIC
STATUS:CONFIRMED
CATEGORIES:Biology,Bsbsigns
LOCATION:Biological Sciences Building - 1060
CONTACT:
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