Yang Yang Flyer by uscbiscgrad on Scribd
Showing posts with label MOL. Show all posts
Showing posts with label MOL. Show all posts
Monday, March 9, 2020
Sunday, February 23, 2020
Monday, February 17, 2020
Monday, February 10, 2020
Sunday, February 2, 2020
Wrigley Sonosky Sustainability summer fellowship
The USC Wrigley Institute is now accepting applications for the 2020 Sonosky Sustainability Summer Fellowship. Applications due March 11. Notice is attached.
Sonosky 2020 Announcement by uscbiscgrad on Scribd
Monday, January 27, 2020
Tuesday, January 21, 2020
Molecular & Computational Biology Colloquium | Dr. Jacob Musser
Dr. Jacob Musser
Post-Doctoral Fellow, EMBL, Developmental Biology Unit (Heidelberg)
Research Profile | Abstract
Few cell types, many functions: The evolutionary origin of division of labor among animal cells
Thursday, January 23, 10:30-11:45 AM, RRI 101
Abstract: Sponges are the sister group to nearly all other animals, and lack a nervous system, musculature, and gut. However, genes encoding important neuronal proteins, including key synaptic proteins, have been found in sponge genomes. Using single-cell RNAseq, single-molecule FISH, and Focused Ion Beam SEM (FIB-SEM) we generate a comprehensive molecular and morphological characterization of cell types in Spongilla lacustris, a freshwater demosponge. We identify many specialized cell types bearing functional and regulatory signatures similar to those of other animals. This includes contractile epithelial cells, which we demonstrate experimentally are responsive to nitric oxide signaling, phagocytes involved in innate immunity, and digestive cells that express a nearly complete set of postsynaptic genes. Remarkably, we also find immune cells expressing presynaptic genes and show via FIB-SEM that they send long projections that directly contact and enwrap microvilli of 'postsynaptic' digestive cells. This reveals new evidence linking neuronal and immune function in sponges, and suggests a primordial neuro-immune system cleared intruders and controlled ciliary beating for feeding.
Post-Doctoral Fellow, EMBL, Developmental Biology Unit (Heidelberg)
Research Profile | Abstract
Few cell types, many functions: The evolutionary origin of division of labor among animal cells
Thursday, January 23, 10:30-11:45 AM, RRI 101
Abstract: Sponges are the sister group to nearly all other animals, and lack a nervous system, musculature, and gut. However, genes encoding important neuronal proteins, including key synaptic proteins, have been found in sponge genomes. Using single-cell RNAseq, single-molecule FISH, and Focused Ion Beam SEM (FIB-SEM) we generate a comprehensive molecular and morphological characterization of cell types in Spongilla lacustris, a freshwater demosponge. We identify many specialized cell types bearing functional and regulatory signatures similar to those of other animals. This includes contractile epithelial cells, which we demonstrate experimentally are responsive to nitric oxide signaling, phagocytes involved in innate immunity, and digestive cells that express a nearly complete set of postsynaptic genes. Remarkably, we also find immune cells expressing presynaptic genes and show via FIB-SEM that they send long projections that directly contact and enwrap microvilli of 'postsynaptic' digestive cells. This reveals new evidence linking neuronal and immune function in sponges, and suggests a primordial neuro-immune system cleared intruders and controlled ciliary beating for feeding.
Sunday, November 4, 2018
Monday, October 29, 2018
Sunday, September 30, 2018
Sunday, September 16, 2018
Sunday, September 9, 2018
Monday, April 2, 2018
Molecular Biology Seminar
Vicki Lundblad
Salk Institute for Biological Studies
Profile
A new model for telomerase: replication fork collapse drives telomere length homeostasis
Friday, April 6
12:00 PM
RRI 101
Abstract: Telomeres, the natural ends of linear chromosomes, must be replenished by the enzyme telomerase to ensure continuous proliferation of cells. The prevailing model in the field assumes that telomerase elongates chromosome termini only after DNA replication is complete. Dr. Lundblad will propose that the major substrate for telomerase is instead generated by errors that occur during replication of duplex telomeric DNA..
Host: Oscar Aparicio
Salk Institute for Biological Studies
Profile
A new model for telomerase: replication fork collapse drives telomere length homeostasis
Friday, April 6
12:00 PM
RRI 101
Abstract: Telomeres, the natural ends of linear chromosomes, must be replenished by the enzyme telomerase to ensure continuous proliferation of cells. The prevailing model in the field assumes that telomerase elongates chromosome termini only after DNA replication is complete. Dr. Lundblad will propose that the major substrate for telomerase is instead generated by errors that occur during replication of duplex telomeric DNA..
Host: Oscar Aparicio
Monday, March 26, 2018
Molecular Biology Seminar Series
Dr. Gavin Sherlock
Stanford University,
Lab Website
“Exploring the Join Distribution of Fitness Effects for Beneficial Mutations in Yeast.”
Friday, March 30, 2018
12:00 PM
RRI 101
Abstract: We previously developed a lineage tracking system to follow the dynamics of adaptive evolution of 500,000 isogenic haploid lineages of Saccharomyces cerevisiae under a glucose limited regime. By tracking the lineage tags over time, we showed that ~20,000 of the lineages gained a beneficial mutation during the experiment, which occurs over only 240 generations. Furthermore, we have also been able to generate a distribution of fitness effects for these lineages (Levy, Blundell et al, Nature (2015)). We isolated thousands of clones belonging to specific lineages, remeasured their fitness, and whole genome sequenced ~120 haploid clones from independent lineages that had gained beneficial mutations. We found that the RAS/cAMP/PKA pathway and the Tor pathway are frequently targets for adaptation under our conditions, uncovering almost 80 mutations in these pathways. In several cases where a gene has a paralog, beneficial mutations are recovered in one paralog significantly more frequently than that other. We have also found that even when mutations affect the same pathway, that the fitness conferred by mutations in a given gene tends to be specific for that gene, and distinct from the fitness effect of mutations in other genes in the pathway (Venkataram et al, Cell (2016)).
We next measured the fitness of these lineages under alternative conditions to determine in what phase of the growth cycle the beneficial mutations provide their fitness benefit, and whether there are within growth cycle fitness tradeoffs. By extending or shortening the length of exponential phase or stationary phase, we found that lineages carrying mutations from the same pathway show similar patterns of fitness change. Furthermore, Ras pathway mutants accrue fitness from spending time in the respiratory growth phase, but this fitness benefit is only manifested in the next growth cycle, as a shortening of lag phase. We also find that these mutants show deleterious effects in stationary phase, suggesting intrinsic tradeoffs between different parts of the growth cycle (Li et al., Current Biology (2018)).
Finally, to generalize beyond closely related experimental conditions, we have evolved both haploid and diploid yeast in several environments, using a double barcode approach, wherein the evolution condition is encoded in the second barcode. We have isolated adaptive clones from each of the conditions, then pooled them, and remeasured their fitness across each of the conditions, to understand how the ways in which beneficial mutants may either be generalists or specialists, and the ways in which they might tradeoff.
Stanford University,
Lab Website
“Exploring the Join Distribution of Fitness Effects for Beneficial Mutations in Yeast.”
Friday, March 30, 2018
12:00 PM
RRI 101
Abstract: We previously developed a lineage tracking system to follow the dynamics of adaptive evolution of 500,000 isogenic haploid lineages of Saccharomyces cerevisiae under a glucose limited regime. By tracking the lineage tags over time, we showed that ~20,000 of the lineages gained a beneficial mutation during the experiment, which occurs over only 240 generations. Furthermore, we have also been able to generate a distribution of fitness effects for these lineages (Levy, Blundell et al, Nature (2015)). We isolated thousands of clones belonging to specific lineages, remeasured their fitness, and whole genome sequenced ~120 haploid clones from independent lineages that had gained beneficial mutations. We found that the RAS/cAMP/PKA pathway and the Tor pathway are frequently targets for adaptation under our conditions, uncovering almost 80 mutations in these pathways. In several cases where a gene has a paralog, beneficial mutations are recovered in one paralog significantly more frequently than that other. We have also found that even when mutations affect the same pathway, that the fitness conferred by mutations in a given gene tends to be specific for that gene, and distinct from the fitness effect of mutations in other genes in the pathway (Venkataram et al, Cell (2016)).
We next measured the fitness of these lineages under alternative conditions to determine in what phase of the growth cycle the beneficial mutations provide their fitness benefit, and whether there are within growth cycle fitness tradeoffs. By extending or shortening the length of exponential phase or stationary phase, we found that lineages carrying mutations from the same pathway show similar patterns of fitness change. Furthermore, Ras pathway mutants accrue fitness from spending time in the respiratory growth phase, but this fitness benefit is only manifested in the next growth cycle, as a shortening of lag phase. We also find that these mutants show deleterious effects in stationary phase, suggesting intrinsic tradeoffs between different parts of the growth cycle (Li et al., Current Biology (2018)).
Finally, to generalize beyond closely related experimental conditions, we have evolved both haploid and diploid yeast in several environments, using a double barcode approach, wherein the evolution condition is encoded in the second barcode. We have isolated adaptive clones from each of the conditions, then pooled them, and remeasured their fitness across each of the conditions, to understand how the ways in which beneficial mutants may either be generalists or specialists, and the ways in which they might tradeoff.
Sunday, March 18, 2018
Molecular Biology Seminar Series
Dr. Adriana Bankston
Future of Research
Personal website
Making postdocs “less invisible” in academia
Friday, March 23, 2018
12:00 PM
RRI 101
Abstract: Future of Research (FoR) aims to champion, engage and empower early career scientists with evidence-based resources to improve the scientific research endeavor. As part of this goal, we study academic policies that affect postdocs. Postdocs make up a large portion of the biomedical workforce. However, they are typically considered the “invisible” population in academia. Lack of data on postdoc numbers, titles and pay contributes to the difficulty of devising novel, or improving existing, policies for postdocs. Our studies examined national postdoc trends in these areas. We monitored institutional postdoc salary policies as a result of labor law changes; obtained actual postdoc salaries in U.S. public institutions; and found large institutional variability in reporting postdoc numbers in an established NSF survey. Given these findings, we call for better measures to assess postdoc population trends. We hope these efforts will make postdocs a “less invisible” population, and contribute to an overall recognition of the need for increased academic transparency.
Future of Research
Personal website
Making postdocs “less invisible” in academia
Friday, March 23, 2018
12:00 PM
RRI 101
Abstract: Future of Research (FoR) aims to champion, engage and empower early career scientists with evidence-based resources to improve the scientific research endeavor. As part of this goal, we study academic policies that affect postdocs. Postdocs make up a large portion of the biomedical workforce. However, they are typically considered the “invisible” population in academia. Lack of data on postdoc numbers, titles and pay contributes to the difficulty of devising novel, or improving existing, policies for postdocs. Our studies examined national postdoc trends in these areas. We monitored institutional postdoc salary policies as a result of labor law changes; obtained actual postdoc salaries in U.S. public institutions; and found large institutional variability in reporting postdoc numbers in an established NSF survey. Given these findings, we call for better measures to assess postdoc population trends. We hope these efforts will make postdocs a “less invisible” population, and contribute to an overall recognition of the need for increased academic transparency.
Tuesday, February 20, 2018
Molecular Biology Seminar Series
Zach Pincus
Washington University in St. Louis.
Lab Website
Live Fast, Die Young: Long Life and Good Health in C. elegans.
Friday, February 23, 2018
12:00 PM
RRI 101
Abstract: My lab seeks to understand why some individuals live longer and/or healthier lives than others. Within a genetically identical population, long- vs. short-lived C. elegans diverge early in adulthood. The first observable differences are in expression of key regulatory microRNAs. Subsequently, physiological function diverges as well. While short-lived individuals experience more rapid declines in physiological health ("live fast, die young"), long-lived individuals systematically outlive their span of good health and experience an "extended twilight" of low function. Last, we find that only select longevity mutants alter this relationship between lifespan and healthspan.
Washington University in St. Louis.
Lab Website
Live Fast, Die Young: Long Life and Good Health in C. elegans.
Friday, February 23, 2018
12:00 PM
RRI 101
Abstract: My lab seeks to understand why some individuals live longer and/or healthier lives than others. Within a genetically identical population, long- vs. short-lived C. elegans diverge early in adulthood. The first observable differences are in expression of key regulatory microRNAs. Subsequently, physiological function diverges as well. While short-lived individuals experience more rapid declines in physiological health ("live fast, die young"), long-lived individuals systematically outlive their span of good health and experience an "extended twilight" of low function. Last, we find that only select longevity mutants alter this relationship between lifespan and healthspan.
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