Showing posts with label behavior. Show all posts
Showing posts with label behavior. Show all posts

July 5, 2012

I’ve never run a marathon, but I’d imagine that it is a rollercoaster of feelings that finishes with a life “high” that is unbeatable. That’s how I feel when I read a paper from the journal Cell. They’re long, exhausting, sweat-inducing, and frequently some of the most rewarding paper-reading experiences a biologist can have. Today’s image is from a Cell paper that is so extensive in data, with a story that starts with protein localization and ends with a behavior study in mice.

Fibroblast growth factors (FGFs) are proteins that regulate several processes during development, such blood vessel growth and neurogenesis. A research group recently investigated the developmental role of FGF13, a growth factor believed to be connected to X-chromosome-linked mental retardation. Wu and colleagues found that FGF13 interacts with and stabilizes microtubules in cerebral cortical neurons during development. Through this interaction, FGF13 is required to polarize neurons—an event necessary for proper neuron migration and brain development. Finally, Wu and colleagues tracked the behavior of mice lacking FGF13, and found a reduced learning ability similar to that seen in X-chromosome-linked mental retardation patients. Images above show control (left) and FGF13-silenced (right) neurons in cerebral cortical slices. Without FGF13, neurons could not complete their radial migration in the tissue.

ResearchBlogging.orgWu QF, Yang L, Li S, Wang Q, Yuan XB, Gao X, Bao L, & Zhang X (2012). Fibroblast growth factor 13 is a microtubule-stabilizing protein regulating neuronal polarization and migration. Cell, 149 (7), 1549-64 PMID: 22726441
 Copyright ©2012 Elsevier Ltd. All rights reserved.

October 31, 2011


All storytellers want to tell their story all the way to its end. Imagine how unsatisfying most movies or books would be without their endings. What if Scout didn’t get to meet Boo Radley? How boring would
The Sixth Sense be? How tragic would Toy Story 3 be?! In cell biology, telling a whole story in one paper, from protein to cell to animal, is a rare luxury given the time and difficulty of most techniques. Today’s image is from a paper with a well-rounded story about the role of a cell cycle protein in non-cell cycle-related business.

The cell cycle is driven forward by complexes made up of proteins called cyclins and cyclin-dependent kinases (Cdks). One cyclin called cyclin E functions in the G1 to S phase transition in the cell cycle, marking the start of DNA replication. Because of this role, cyclin E is typically found in only dividing cells. A recent paper describes the important role of cyclin E in non-dividing cells in the adult brain. In this paper, Odajima and colleagues found that cyclin E regulates synapse formation by inhibiting Cdk5. Cyclin E disruption in neurons causes the number of synapses and dendritic spines to drop. Finally, adult mice with cyclin E-deficient brains had impaired learning and memory. In the images above, non-dividing neurons from mouse brain show the presence of cyclin E (red) in both axons and dendrites, along with Cdk5. SynGAP and Synapsin I are post- and presynaptic markers.


ResearchBlogging.orgOdajima, J., Wills, Z., Ndassa, Y., Terunuma, M., Kretschmannova, K., Deeb, T., Geng, Y., Gawrzak, S., Quadros, I., Newman, J., Das, M., Jecrois, M., Yu, Q., Li, N., Bienvenu, F., Moss, S., Greenberg, M., Marto, J., & Sicinski, P. (2011). Cyclin E Constrains Cdk5 Activity to Regulate Synaptic Plasticity and Memory Formation Developmental Cell, 21 (4), 655-668 DOI: 10.1016/j.devcel.2011.08.009
Copyright ©2011 Elsevier Ltd. All rights reserved.

August 22, 2011

There are some images that just stick with you. They might be beautiful, fascinating, or terrifying. For example, I’ll never forget when my former labmates told me to Google pictures of a teratoma. Seriously, don’t do it…wait, you just did, didn’t you? Unless you are a C. elegans worm, you won’t find today’s images terrifying…instead, you are likely to be utterly fascinated.

C. elegans are small 1mm-long roundworms that are used extensively in biology research. When the head of one of these worms is touched, its immediate response is to quickly back away from the touch. A recent paper describes how a fungus may have shaped the evolution of this behavior. Maguire and colleagues found that a predacious fungus called D. doedycoides capture larval stage worms by forming rings that constrict the worm passes through. There is a delay between when the fungus senses a worm passing through its ring and when it constricts to trap the worm. During this delay, the worm’s touch response can trigger the worm to quickly back out of the trap. However, there are some worms with mutations in its touch response—these worms are caught more efficiently by the fungus. Images above are electron micrographs of larval stage worms caught by the constricting rings of the fungus (left) and close-up images of the fungus’ rings before (top) and after (bottom) they are constricted.

BONUS!! Check out the authors’ video abstract, which includes movies of this predator-prey interaction, here.

ResearchBlogging.orgMaguire, S., Clark, C., Nunnari, J., Pirri, J., & Alkema, M. (2011). The C. elegans Touch Response Facilitates Escape from Predacious Fungi Current Biology, 21 (15), 1326-1330 DOI: 10.1016/j.cub.2011.06.063
Copyright ©2011 Elsevier Ltd. All rights reserved.