March 27, 2014

You might think of your bones as unchanging, but they are far more dynamic than you think. Today’s image is from a paper identifying a new blood vessel subtype found in the mouse skeletal system.

Osteogenesis is the formation of new bone tissue, and is important in bone renewal and fracture healing. Recent work suggests that osteogenesis may depend on the presence of blood vessels. A recent paper identified a new capillary subtype found in the mouse skeletal system. Kusumbe and colleagues found that these microvessels mediate growth of bone vasculature, and couple osteogenesis with angiogenesis (the formation of new blood vessels). These vessels and their associated osteoprogenitors were reduced in older bone, yet the reversal of this decline allowed bone mass renewal. In the images above, the microvessels (green) have a branched organization in a juvenile mouse tibia (arrowheads point to interconnections).

Kusumbe, A., Ramasamy, S., & Adams, R. (2014). Coupling of angiogenesis and osteogenesis by a specific vessel subtype in bone Nature, 507 (7492), 323-328 DOI: 10.1038/nature13145
Adapted by permission from Macmillan Publishers Ltd, copyright ©2014

March 19, 2014

Migration fingers are the spirit fingers of a migrating epithelial sheet of cells. Woowoo!! Today’s image is from a cool paper on the forces exerted by a migration finger, so naturally I’m showing my enthusiasm with my own spirit fingers.

Cells can migrate on their own or as part of an epithelial sheet of many cells. Collective migration features the forward movement of multicellular migration fingers, and can be seen throughout development, in spreading tumors and in healing wounds. The formation of each migration finger begins with the transformation of a single cell into a leader cell. A recent paper looks at leader cells and migration fingers, specifically the biochemical mechanisms involved and the generation of forces exerted by migration fingers. Reffay and colleagues monitored the traction forces exerted by a migration finger, and found that the leader cell exerts a large mechanical force that drags its followers with the help of the small GTPase RhoA. In the images above, the contractile acto-myosin cable that runs the length of the migration finger is cut by laser photoablation (arrow, middle). A new leader cell is formed at the site of the cut (asterisk, right), suggestion that the cable serves to prevent the formation of new leader cells, which in turn allows the formation of long migration fingers.


Reffay, M., Parrini, M., Cochet-Escartin, O., Ladoux, B., Buguin, A., Coscoy, S., Amblard, F., Camonis, J., & Silberzan, P. (2014). Interplay of RhoA and mechanical forces in collective cell migration driven by leader cells Nature Cell Biology, 16 (3), 217-223 DOI: 10.1038/ncb2917
Adapted by permission from Macmillan Publishers Ltd, copyright ©2014

March 12, 2014

I love a lot of things that are rings, especially donuts. Turns out, though, that ring chromosomes are terrible news. A recent paper shows the loss of ring chromosomes when cells are reprogrammed, suggesting possible ‘chromosome therapy’ through cell reprogramming.

Ring chromosomes form when the two arms of a chromosome fuse, and are sometimes associated with large terminal deletions. These ring chromosomes lead to birth defects, mental disabilities, and growth retardation. Unfortunately, there are no treatments for ring chromosome disorders due the severity of the aberrations. In a recent study, Bershteyn and colleagues generated induced pluripotent stem cells (iPSCs) from cells of a Miller Dieker Syndrome patient with large deletions on ring chromosome 17. The induced stem cells lost the ring chromosome and duplicated the normal homologous chromosome through a mechanism called compensatory uniparental disomy. The images above show two karyotypes—one with the ring chromosome 17 (left, inset), and one without (right).

Bershteyn, M., Hayashi, Y., Desachy, G., Hsiao, E., Sami, S., Tsang, K., Weiss, L., Kriegstein, A., Yamanaka, S., & Wynshaw-Boris, A. (2014). Cell-autonomous correction of ring chromosomes in human induced pluripotent stem cells Nature, 507 (7490), 99-103 DOI: 10.1038/nature12923
Adapted by permission from Macmillan Publishers Ltd, copyright ©2014

March 5, 2014

Mitochondria are the cellular power plants, but bigger power plants are not always a good thing. Defects in the regulation of mitochondrial size and dynamics can cause neurodegenerative diseases such as Alzheimer’s disease. Today’s image is from a paper describing an important player in mitochondrial division, or fission.

Mitochondria serve as the cellular power plants due to their production of ATP, the cell’s energy source, and are quite dynamic, with fusion and fission events occurring regularly. Mitochondrial fission is how mitochondria divide, but fission also plays an important role in apoptosis and ridding the cell of damaged mitochondrial components. In current models of fission, the GTPase dynamin (Drp1) forms a ring around and constricts the mitochondrial membranes. A recent paper describes the importance of the myosin II, an actin motor, in Drp1-mediated fission. Korobova and colleagues found that inhibition of myosin II resulted in abnormally long mitochondria. This inhibition of myosin II also affected the presence of Drp1 at mitochondria. In the images above, the use of blebbistatin, a myosin II chemical inhibitor, resulted in long mitochondria (right), compared to control mitochondria (left).

Korobova, F., Gauvin, T., & Higgs, H. (2014). A Role for Myosin II in Mammalian Mitochondrial Fission Current Biology, 24 (4), 409-414 DOI: 10.1016/j.cub.2013.12.032
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