Teaching to Learn: iPads as Tools for Transforming Physics Student Roles

Students who serve as Learning Assistants (LAs) and have the opportunity to teach the content they are learning, while also studying effective teaching pedagogy, have demonstrated achievement gains in advanced content courses and positive shifts in attitudes about learning science [V. Otero, S. Pollock & N. Finkelstein, Amer J Physics 78, 11 (2010)]. Although the LA experience is also valuable for high school students, the tight schedule and credit requirements of advanced high school students limit opportunities for implementing traditional LA programs at the high school level. In order to provide high school physics students with an LA-like experience, iPads were used as tools for students to synthesize screencast video tutorials for students to access, review and evaluate. The iPads were utilized in a one-to-one tablet-to-student environment throughout the course of an entire school year. This research investigates the impact of a one-to-one iPad environment and the use of iPads to create teaching-to-learn (TtL) experiences on student agency and attitudes toward learning science. Project funded by NSF grant # DUE 934921.Comment: Proc. 2013 Physics Education Research Conference. AIP Pres

Eps8 Regulates Axonal Filopodia in Hippocampal Neurons in Response to Brain-Derived Neurotrophic Factor (BDNF)

A novel signaling cascade controlling actin polymerization in response to extracellular signals regulates filopodia formation and likely also neuronal synapse formation

Effects of embedded anomlies and oral reading errors on children's understanding of stories

Includes bibliographical references (p. 25-26)Supported in part by the National Institute of Education under contract no. US-NIE-C-400-76-011

Actin Dynamics: Growth from Dendritic Branches

The dendritic nucleation model was devised to explain the cycle of actin dynamics resulting in actin filament network assembly and disassembly in two contexts — at the leading edge of motile cells and in the actin comet tails of intracellular pathogenic bacteria and viruses. Due to the detailed nature of its biochemical predictions, the model has provided an excellent focus for subsequent experimentation. This review summarizes recent work on actin dynamics in the context of the dendritic nucleation model. One outcome of this research is the possibility that additional proteins, as well as the six proteins included in the original model, might increase the efficiency of dendritic nucleation or modify the resulting actin network. In addition, actin dynamics at the leading edge might be influenced by a second actin filament network, independent of dendritic nucleation

The Arp2/3 inhibitory protein arpin induces cell turning by pausing cell migration

International audienceBranched actin networks generated by the Arp2/3 complex provide the driving force for leading edge protrusion in migrating cells. We recently identified Arpin, a protein that inhibits the Arp2/3 complex in lamellipodia. Arpin is activated by the small GTPase Rac, which triggers lamellipodium formation, and thus Arpin renders protrusions unstable. A conserved role of Arpin is to induce migrating cells to turn in different migration models. Here we investigated the mechanism by which Arpin controls directional persistence. For this analysis, we segmented migration trajectories into alternating phases of active migration and pauses, based on a speed threshold. Regardless of the threshold value, Arpin induced more frequent pausing, during which the cell was more likely to change the direction of its migration. Arpin simultaneously acts on cell speed and directional persistence, which are strongly coupled parameters. Induction of frequent pausing by Arpin is consistent with Arpin circuitry: by inhibiting the Arp2/3 complex as a response to Rac activation, Arpin antagonizes a positive feedback loop that sustains protrusions at the leading edge and maintains active migration. We propose the duration of active migration' as a useful proxy to measure feedbacks associated with cell migration. (c) 2015 Wiley Periodicals, Inc

Gadkin negatively regulates cell spreading and motility via sequestration of the actin-nucleating ARP2/3 complex

Regulation of actin dynamics is key to many cell physiological processes, ranging from protrusion formation and control of cell shape to cellular motility, endocytosis, and vesicle movement. The actin-related protein (ARP)2/3 complex is a major actin nucleator organizing branched filament networks in lamellipodial protrusions and during cell migration downstream of nucleation-promoting factors (NPFs). Although many NPFs have been characterized in detail, only few ARP2/3 inhibitors are known. Here, we identify the trans-Golgi network (TGN)/endosomally localized adaptor protein (AP)-1-associated adaptor protein Gadkin as a negative regulator of ARP2/3 function. Loss of Gadkin is associated with a partial redistribution of ARP2/3 to the plasma membrane and with increased cell spreading and migration, phenotypes that depend on the presence of a functional ARP2/3 complex. Gadkin directly binds to ARP2/3 via a conserved tryptophan-based acidic cluster motif reminiscent of ARP2/3-binding sequences of NPFs but fails to facilitate ARP2/3-mediated actin assembly. Consistent with an inhibitory role of Gadkin on ARP2/3 function, ARP2/3 is found on motile Gadkin-containing endosomal vesicles under migration-inhibiting conditions from where it relocalizes to the plasma membrane following activation of NPFs. Together with the observation that Gadkin-mediated inhibition of cell spreading requires its binding to ARP2/3, these data indicate that Gadkin is a negative regulator of ARP2/3 function present on intracellular membranes

Actin-based protrusions of migrating neutrophils are intrinsically lamellar and facilitate direction changes.

Leukocytes and other amoeboid cells change shape as they move, forming highly dynamic, actin-filled pseudopods. Although we understand much about the architecture and dynamics of thin lamellipodia made by slow-moving cells on flat surfaces, conventional light microscopy lacks the spatial and temporal resolution required to track complex pseudopods of cells moving in three dimensions. We therefore employed lattice light sheet microscopy to perform three-dimensional, time-lapse imaging of neutrophil-like HL-60 cells crawling through collagen matrices. To analyze three-dimensional pseudopods we: (i) developed fluorescent probe combinations that distinguish cortical actin from dynamic, pseudopod-forming actin networks, and (ii) adapted molecular visualization tools from structural biology to render and analyze complex cell surfaces. Surprisingly, three-dimensional pseudopods turn out to be composed of thin (<0.75 µm), flat sheets that sometimes interleave to form rosettes. Their laminar nature is not templated by an external surface, but likely reflects a linear arrangement of regulatory molecules. Although we find that Arp2/3-dependent pseudopods are dispensable for three-dimensional locomotion, their elimination dramatically decreases the frequency of cell turning, and pseudopod dynamics increase when cells change direction, highlighting the important role pseudopods play in pathfinding