October 28, 2014

If you’ve ever tried to get your kids to share a donut, you understand the importance to dividing things equally (and learning crucial lessons…just buy more donuts next time...I mean, seriously!). Cell division is no different—chromosomes and organelles must all get divided equally. Today’s images are from a paper showing how mitochondria are positioned during cell division in order to allow equal segregation.

Many years of research have focused on the equal segregation of chromosomes during cell division. Organelles such as mitochondria must also be segregated equally in a dividing cell, and errors in this process can lead to disease. A recent paper identifies the actin motor Myosin-XIX (Myo19) as a key player in mitochondrial partitioning during cell division. Myo19 is localized to mitochondria, and cells depleted of Myo19 have an abnormal distribution of mitochondria. Rohn and colleagues found that cells lacking Myo19 experience stochastic division failure, suggesting that mitochondria are physically preventing successful cell division. The images above show dividing cells labeled to visualize mitochondria (green) and the mitotic spindle (red) in control cells (top two rows) and cells depleted of Myo19 (bottom two rows). Without Myo19, mitochondria moved towards spindle poles at the onset of anaphase, causing an asymmetric distribution at division when compared with control cells.

BONUS!! Here is a rotating 3D reconstruction of an A549 stained to visualize microtubules (green), mitochondria (red), and DNA (blue). Omar Quintero, HighMag friend and a co-author from today’s paper, loves this image: “I like it because it reminds me of the scenes in StarWars where the Rebels are planning their attack on the Death Star.”

Rohn, J., Patel, J., Neumann, B., Bulkescher, J., Mchedlishvili, N., McMullan, R., Quintero, O., Ellenberg, J., & Baum, B. (2014). Myo19 Ensures Symmetric Partitioning of Mitochondria and Coupling of Mitochondrial Segregation to Cell Division Current Biology DOI: 10.1016/j.cub.2014.09.045

Copyright ©2014 Elsevier Ltd. All rights reserved.

October 24, 2014

There is a party going on at the ends of microtubules, but I wasn’t invited. That won’t stop me, or countless cell biologists out there, from peeping in the window to check out all of the microtubule shenanigans. Today’s image is from a paper describing how Doublecortin binds to microtubule ends.

The plus end of a microtubule is the primary site for growth and shrinkage, and interaction with several microtubule-associate proteins. Different microtubule end-binding proteins may interact with microtubules using different mechanisms: the end-binding protein EB1 relies on the nucleotide state of the tubulin at the microtubule end, while a recent paper shows how another protein, Doublecortin (DCX), relies on the curvature of microtubule ends for binding. DCX is a neuronal microtubule-associate protein that plays an important role throughout development, yet how it interacted with microtubule ends was previously unclear. Bechstedt and colleagues used single-molecule microscopy to show that DCX (images above, green in merged) binds with higher affinity to curved microtubules (magenta) than to straight microtubules. DCX mutations, which are found in patients with double cortex syndrome, prevent the protein from binding to curved regions of microtubules.

Bechstedt, S., Lu, K., & Brouhard, G. (2014). Doublecortin Recognizes the Longitudinal Curvature of the Microtubule End and Lattice Current Biology, 24 (20), 2366-2375 DOI: 10.1016/j.cub.2014.08.039
Copyright ©2014 Elsevier Ltd. All rights reserved.


October 17, 2014

For years, the prettiest cells to image were flat cells in a dish. Thanks to the tireless work of many, beautiful high-resolution images can now come from tissue within a living organism. Today’s image is from a paper showing improved techniques for imaging fine cellular processes within large volumes, from the lab of recent Nobel prize winner, Eric Betzig. 

A material’s refractive index refers to how light travels through it; the simplest example being how light bends when passed through water. The refractive index heterogeneities stemming from the many cell types, morphologies, and subdomains within a living organism are a challenge to microscopists. As described in a paper from earlier this year, Wang and colleagues improved on previous techniques for imaging within large volumes. Wang and colleagues use adaptive optics (AO), which corrects for the microscope’s aberrations that limit image resolution, in a mode fast enough to correct for the various aberrations within a large sample, without inducing photodamage or photobleaching. The image above shows a 3D rendering from deep within a living zebrafish brain, with oligodendrocytes (magenta) and neuronal nuclei (green) visible.

Wang, K., Milkie, D., Saxena, A., Engerer, P., Misgeld, T., Bronner, M., Mumm, J., & Betzig, E. (2014). Rapid adaptive optical recovery of optimal resolution over large volumes Nature Methods, 11 (6), 625-628 DOI: 10.1038/nmeth.2925
Adapted by permission from Macmillan Publishers Ltd, copyright ©2014

Nobel, Nobel, Nobel!!!!

Last week the Chemistry Nobel Prize went to three amazing biologists who have been steadily and remarkably improving the world of imaging.  Eric Betzig, Stefan Hell, and W.E. Moerner made Abbe's diffraction limit a mere hurdle to leap over, not a finish line.  We'll feature some work from Eric Betzig's lab later in the week, but until then check out the links below:

Great popular science descriptions of Betzig, Hell, and Moerner's accomplisments:
Beaming with Pride - From Slate, by Boer Deng
How the optical microscope became a nanoscope - Popular Science Background from the Royal Swedish Academy of Sciences

We've featured work from Eric Betzig before:  here and here.
We've also featured stunning images using STORM: here.

October 9, 2014

As Tom and Jerry have proven time and time again, repulsive forces are serious business and highly entertaining. Today’s image is from a paper describing how different cell types repel one another to help create boundaries between tissues. 

The study of how cells adhere to or repel one another is an important field of study in developmental biology. Ephrin ligands and their respective Eph receptors trigger repulsive cues between cells of different types. Many different tissue types express the same ephrins and Eph receptors, yet only those cells at the tissue interface repel one another. A recent study tests how these signals are integrated to provide repulsion at only the tissue interface, and not between cells of the same tissue. Rohani and colleagues used the dorsal ectoderm-mesoderm boundary of early frog embryos to find Eph-ephrin pairs that are expressed in complementary tissues. The cells at the boundary of the tissues have a combined Eph-ephrin repulsive signal that is sufficient for a repulsive force, suggesting a simple model of repulsion based on relative concentrations and binding affinities of Eph receptors and ephrins at tissue boundaries. The image above shows the higher concentration of EphB receptors (green) at the ectoderm-mesoderm boundary.

Rohani, N., Parmeggiani, A., Winklbauer, R., & Fagotto, F. (2014). Variable Combinations of Specific Ephrin Ligand/Eph Receptor Pairs Control Embryonic Tissue Separation PLoS Biology, 12 (9) DOI: 10.1371/journal.pbio.1001955