January 29, 2014

The term “pathogen propulsion” sounds like an awesome technique for defeating the evil squid overlords. In fact, a lot of concepts involving propulsive actin comets sound awesomely science fictional, but thankfully they are not. Today’s image is from a paper describing how several viruses use actin comet tails to propel themselves to other cells.

Several pathogens such as baculovirus, Listeria, and Shigella hijack their host cell’s own actin cytoskeleton in order to propel themselves into other cells and spread infection. Behind each pathogen is a comet made of actin filaments and associated actin regulators, but the mechanism of propulsion and the structure of the actin comet have been debated. A recent paper in PLoS Biology by Mueller and colleagues describes the use of electron tomography to show a fishbone-like array of actin filaments behind baculovirus, the smallest pathogen known to use propulsive actin comets. These comets use an average of four actin filaments at any one time to propel the virus. Using these results, the researchers ran computer simulations that support a model of propulsion in which actin filaments are continuously tethered to the pathogen. The image above shows a negatively-stained actin comet tail behind a baculovirus particle (BV), and the 3D projection of the image shows branch points of the actin tail as red dots. Insets in top image show details of the branch points, and grey tube is a microtubule.

BONUS! Below is a movie of baculovirus propelling itself around a cell. Virus particles are red, and actin comet tails can be seen in green behind the particles.

Mueller J, Pfanzelter J, Winkler C, Narita A, Le Clainche C, et al. (2014) Electron Tomography and Simulation of Baculovirus Actin Comet Tails Support a Tethered Filament Model of Pathogen Propulsion. PLoS Biol 12(1): e1001765. doi:10.1371/journal.pbio.1001765.

January 22, 2014

The C-word is a dirty, dirty word that every single person dreads hearing. Cancer touches every family at some point (or so it seems), so the effort put forth to finding a “cure” for cancer is huge. Today’s image is from a very exciting paper that shows how specific cells in a breast tumor lead the charge towards invasion. 

The spread of cancer, or metastasis, can occur either through the invasion of single tumor cells into nearby tissue or by collective invasion of several cells as a cohesive unit. A recent paper from Andy Ewald’s lab at Johns Hopkins describes the identification of cells involved in collective invasion, using a 3D assay of primary breast tumors invading other tissue. Kevin Cheung and colleagues found that in mouse breast cancer models and diverse human breast tumors, the cells leading the invasion charge are distinct from the bulk tumor cells, and express the basal epithelial genes cytokeratin-14 (K14) and p63. Additionally, knockdown of either K14 or p63 could block collective invasion in advanced carcinomas. In the images above, leading invasive cells express K14 (middle image, green) and are distinct from the bulk of the mouse mammary tumor.

BONUS!! For a great “Out of the Box” description of these very cool results, click here.

Kevin J. Cheung, Edward Gabrielson, Zena Werb, Andrew J. Ewald (2013).  Collective Invasion in Breast Cancer Requires a Conserved Basal Epithelial Program.  Cell, 15 (7), 1639–1651. http://dx.doi.org/10.1016/j.cell.2013.11.029  Copyright ©2013 Elsevier Ltd. All rights reserved.

January 15, 2014

The mitotic spindle seems to get all the fun of a microtubule-dynein party, but do not fret. A recent paper describes some cool interactions of microtubules with dynein at the cell’s cortex.

The molecular motor dynein walks along microtubules, and this movement can do great things by moving the microtubules themselves or moving material along the microtubule. Recent work found that dynein at the cell’s cortex may influence cell motility using an actin-independent mechanism that pushes microtubules along the cortex. In an even more recent paper in the journal Molecular Biology of the Cell, this same research group shows these cortical dynein-microtubule interactions directly. Using TIRF microscopy, Mazel and colleagues found speckles of cortical dynein complexes associated with microtubules. These microtubules can move, bend, and even rotate around these speckles. The images above show the difference between wide-field microscopy (left) and TIRFM (right) when imaging microtubules at the cortex. In the bottom panel, a short microtubule can be seen moving directionally.


Tomáš Mazel, Anja Biesemann, Magda Krejczy, Janos Nowald, Olga Müller, & Leif Dehmelt (2014). Direct observation of microtubule pushing by cortical dynein in living cells Molecular Biology of the Cell, 25 (1) DOI: 10.1091/mbc.E13-07-0376

I’mmmm baaaaaack!

I’mmmm baaaaaack!

It’s a new year for HighMag Blog, and it’s about time for me to get back to the wondrous world of cells.

On August 12, I welcomed my second daughter into this world and have been spending my time getting to know her. I have to admit that science has been far from my mind as I’ve tried to figure out how to take care of two little ones, but I’m starting to miss cells and their crazy worlds. Next week, I’ll begin posting images (weekly at first). I look forward to again having my 4-year old gape over my shoulder to ask about the images I’m writing about…no age is too young for a journey into the Alberts et al. cell biology bible.

As in the past, I welcome you to submit your own images for a shot at HighMag glamour. I also welcome suggestions for papers/images that you’ve recently come across that absolutely must have their day in the spotlight. Email me at highmagblog@gmail.com.