Comparative Dynamics of Retrograde Actin Flow and Focal Adhesions: Formation of Nascent Adhesions Triggers Transition from Fast to Slow Flow

Dynamic actin network at the leading edge of the cell is linked to the extracellular matrix through focal adhesions (FAs), and at the same time it undergoes retrograde flow with different dynamics in two distinct zones: the lamellipodium (peripheral zone of fast flow), and the lamellum (zone of slow flow located between the lamellipodium and the cell body). Cell migration involves expansion of both the lamellipodium and the lamellum, as well as formation of new FAs, but it is largely unknown how the position of the boundary between the two flow zones is defined, and how FAs and actin flow mutually influence each other. We investigated dynamic relationship between focal adhesions and the boundary between the two flow zones in spreading cells. Nascent FAs first appeared in the lamellipodium. Within seconds after the formation of new FAs, the rate of actin flow decreased locally, and the lamellipodium/lamellum boundary advanced towards the new FAs. Blocking fast actin flow with cytochalasin D resulted in rapid dissolution of nascent FAs. In the absence of FAs (spreading on poly-L-lysine-coated surfaces) retrograde flow was uniform and the velocity transition was not observed. We conclude that formation of FAs depends on actin dynamics, and in its turn, affects the dynamics of actin flow by triggering transition from fast to slow flow. Extension of the cell edge thus proceeds through a cycle of lamellipodium protrusion, formation of new FAs, advance of the lamellum, and protrusion of the lamellipodium from the new base

Some environmental factors influencing phytoplankton in the Southern Ocean around South Georgia

Data on phytoplankton and zooplankton biomass, and physical and chemical variables, are combined with a published multivariate description of diatom species composition to interpret variation within an area around South Georgia surveyed during an austral summer. Large-scale species distributions could be equated to the different water masses which reflected the interaction of the Antarctic Circumpolar Current with the island and the Scotia Ridge. Small-scale factors were found to act at an interstation scale and imposed local variation on the biogeographic pattern. Nutrient depletion could be related to phytoplankton biomass but no single inorganic nutrient of those measured (NO 3 −N, PO 4 −P and silica) could be identified as important. The ratio Si:P appeared to be more important as an ecological factor. The impact of grazing by krill and other zooplankton could only be resolved as differences in phytoplankton biomass and phaeopigment content. Diatom species composition showed a relation to local krill abundance very different from that suggested by published studies, but could be explained as the effect of earlier grazing outside the study area. The effects of vertical mixing could not account for interstation differences as pycnocline depth was uniformly greater than euphotic depth, and vertical stability very low. Some comparison was made with data collected in 1926–31 by the Discovery Investigations. Significant differences in the distribution of certain taxa such as Chaetoceros criophilum and C. socialis were traced to major differences in hydrology.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46983/1/300_2004_Article_BF00443379.pd

Analysis of the Priorities, Obstacles, and Opportunities for Implementing U.S. State Wildlife Action Plans

Introduction and Study Background This report explores the development and implementation of the Comprehensive Wildlife Conservation Strategies, also known as State Wildlife Action Plans (plans), for the nine Northeastern states of Connecticut, Maine, Massachusetts, New Jersey, New York, New Hampshire, Pennsylvania, Rhode Island, and Vermont. As part of a study funded by the National Council for Science and the Environment’s Wildlife Habitat Policy Research Program, eight universities conducted research on development and implementation of all U.S. plans. During 2007–2008, a team of nine interdisciplinary graduate students at the University of Michigan School of Natural Resources and Environment investigated plan development and implementation in nine states in the Northeast United States. This report includes the team’s findings of state wildlife conservation activities, emerging conservation priorities, new conservation approaches and tools, and examples of current projects that demonstrate promising directions for accelerating habitat conservation. What are the State Wildlife Action Plans? In 2001, Congress required states and territories to develop a CWCS in order to continue qualifying for federal State Wildlife Grant funds. Each plan was required to include the following eight common elements: (1) Distribution and abundance of wildlife species, (2) Locations and condition of key habitats and community types, (3) Wildlife and habitat threats, (4) Conservation actions to address these threats, (5) Plans for monitoring species, habitats and the effectiveness of conservation actions, (6) Plans for review and adaptive management of the strategy, (7) Plans to coordinate strategy development, implementation and review with federal, state, local agencies and Indian tribes, and (8) Opportunities for broad public participation in plan development and implementation. While some states approached plan development as an exercise in articulating broad goals and objectives for protecting state species and habitats, others developed more specific action plans with prioritized short-term and long-term actions.Master of ScienceNatural Resources and EnvironmentUniversity of Michiganhttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/21/Regional_ExecSum_Final.dochttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/20/Regional piece_final.dochttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/19/Vermont.dochttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/18/Rhode Island.dochttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/17/Pennsylvania.dochttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/16/New York.dochttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/15/New Jersey.dochttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/14/New Hampshire.dochttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/13/Massachusetts.dochttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/12/Maine.dochttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/11/Connecticut.dochttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/10/EMichael_TransbFreshwater_final.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/9/AppC.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/8/AppB.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/7/AppA.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/6/Visser_Federal%20Collaboration-1.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/5/Lewis%20and%20Theriot_LIP%20final%20report.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/4/Levy.GIS.all.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/3/Lauren_s%20Drilldown%20Final.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/2/Ashley_Partnerships.dochttp://deepblue.lib.umich.edu/bitstream/2027.42/58214/1/Aldridge_Jastremski_DD.pd

Anthrax lethal toxin paralyzes actin-based motility by blocking Hsp27 phosphorylation

Inhalation of anthrax causes fatal bacteremia, indicating a meager host immune response. We previously showed that anthrax lethal toxin (LT) paralyzes neutrophils, a major component of innate immunity. Here, we have found that LT also inhibits actin-based motility of the intracellular pathogen Listeria monocytogenes. LT inhibition of actin assembly is mediated by blockade of Hsp27 phosphorylation, and can be reproduced by treating cells with the p38 mitogen-activated protein (MAP) kinase inhibitor SB203580. Nonphosphorylated Hsp27 inhibits Listeria actin-based motility in cell extracts, and binds to and sequesters purified actin monomers. Phosphorylation of Hsp27 reverses these effects. RNA interference knockdown of Hsp27 blocks LT inhibition of Listeria actin-based motility. Rescue with wild-type Hsp27 accelerates Listeria speed in knockdown cells, whereas introduction of Hsp27 mutants incapable of phosphorylation or dephosphorylation causes slowing down. We propose that Hsp27 facilitates actin-based motility through a phosphorylation cycle that shuttles actin monomers to regions of new actin filament assembly. Our findings provide a previously unappreciated mechanism for LT virulence, and emphasize a central role for p38 MAP kinase-mediated phosphorylation of Hsp27 in actin-based motility and innate immunity