February 28, 2011

A fly may not need to know the temperature in order to decide whether or not to bring a light jacket to dinner, but sensing temperature is important for its survival. A recent paper looks at how fruit flies process temperature.

The antenna of the fruit fly Drosophila is a crucial organ. The antenna can sense many environmental cues, such as sound, wind, and pheromones, that are important for a fly’s survival, and a recent paper adds temperature to this list. Gallio and colleagues map out how temperature is represented in the fly brain and show that there are separate hot and cold neurons in the antenna. Images above show a fly antenna (left) and higher magnification views of the temperature-sensing neurons (right, found in the boxed region of the antenna). The blue response images (bottom) show that the neurons labeled 1 and 2 respond to hot temperatures (left), while the neurons labeled 3 and 4 respond to cold (right).

Gallio, M., Ofstad, T., Macpherson, L., Wang, J., & Zuker, C. (2011). The Coding of Temperature in the Drosophila Brain Cell, 144 (4), 614-624 DOI: 10.1016/j.cell.2011.01.028
Copyright ©2011 Elsevier Ltd. All rights reserved.

February 24, 2011

Don’t assume that two identical-looking cells are the same…they may both be rounded and cute, but there is a lot of exciting stuff brewing inside. A recent paper describes the use of a clever microscopy technique to look at how subtle differences in a transcription factor’s kinetics can predict early patterning in the mouse embryo.

There has always been debate and discussion about when the differences that lead to lineage patterning first appear in the cells of very early embryos. Although cells in the very early mouse embryo appear morphologically identical, a recent paper describes the different kinetics of one transcription factor in different cells in the mouse embryo. To measure these differences, Plachta and colleagues tagged the transcription factor Oct4 with a special fluorescent marker that is activated by a certain wavelength of light. Once this marker was activated in certain cells in the 4- and 8-cell embryo, the movement of Oct4 into and out of the nucleus (where it does its job by binding to DNA) was monitored. One group of cells had slower rates of export and import and was more likely to give rise to the inner cell mass, while the second group had higher rates and was more likely to give rise to the extra-embryonic lineage. Image shows an 8-cell embryo with the Oct4 marker activated (green) in the nucleus of one specific cell.

Plachta, N., Bollenbach, T., Pease, S., Fraser, S., & Pantazis, P. (2011). Oct4 kinetics predict cell lineage patterning in the early mammalian embryo Nature Cell Biology, 13 (2), 117-123 DOI: 10.1038/ncb2154
Adapted by permission from Macmillan Publishers Ltd, copyright 2011

February 21, 2011

Cell migration is a complicated process, and the ease of genetic manipulation in the fruit fly Drosophila makes it an ideal organism for investigating the genes involved. Add some great live imaging to the mix, and you are a big step closer to understanding cell migration.

Border cells are a cluster of migratory cells in the fly egg chamber that are required for proper fertilization of the egg and early patterning of the embryo. This group of 6-10 cells collectively moves to one end of the egg chamber, where the oocyte resides. A recent paper looks at how these cells move collectively by responding to the different guidance cues. These guidance cues affect the formation, size, and productivity of cell extensions that are crucial for migration. Images above show border cells (green) in the egg chamber (left, white line shows the track of one cell during migration). Higher magnification images of the cell cluster (right) show the more streamlined shape of the cluster during the faster early phase of migration, compared with the late phase.

BONUS!! For a verrrrry cool movie of border cell migration, click here. For many great more movies from this paper, click here.

Poukkula, M., Cliffe, A., Changede, R., & Rorth, P. (2011). Cell behaviors regulated by guidance cues in collective migration of border cells originally published in The Journal of Cell Biology, 192 (3), 513-524 DOI: 10.1083/jcb.201010003

February 17, 2011

It may not be intuitive to outsiders, but in order to understand and cure disease, it is crucial to understand development and how an early embryo is built and organized. Today’s image is from a paper clarifying the role of the Alzheimer’s disease-linked gene presenilin in development.

The development of a nervous system is a complex process that requires an extraordinary amount of regulation. In order for neurons and dendrites grow their processes to their final homes and set up the synaptic connections required for normal function, several different guidance proteins must coordinate their signals. A recent paper looks at the role of a protein called Presenilin-1 in the migration of motor neurons in the developing mouse nervous system. Presenilin-1 functions in coordinating the response of a neuron to the different signaling pathways. In the images above, motor axons can been seen (green) in the developing nervous system of mice. In embryos with disrupted Presenilin-1 (right), motor axons can be seen growing past the midline of the floor plate (FP), compared with normal embryos (left). Bottom images are enlarged views of the boxed regions. Images were acquired using an Olympus Fluoview 1000 confocal microscope.

Bai, G., Chivatakarn, O., Bonanomi, D., Lettieri, K., Franco, L., Xia, C., Stein, E., Ma, L., Lewcock, J., & Pfaff, S. (2011). Presenilin-Dependent Receptor Processing Is Required for Axon Guidance Cell, 144 (1), 106-118 DOI: 10.1016/j.cell.2010.11.053
©2011 Elsevier Ltd. All rights reserved.

HighMag turns 1!!

Happy Birthday to HighMag!

Today marks HighMag's first birthday, and I'm beyond thrilled. I want to thank the amazing researchers who have allowed me to share their fabulous images with you. I also want to thank the many journals who have given me permission to use the images appearing on their pages. And, finally, I want to thank HighMag's readers. HighMag started out with one reader (thank you to my husband!), but now boasts many readers and attention from sites such as The Node, EuroStemCell, and ResearchBlogging.

Here are some HighMag stats:
# of images featured - 100 (a wonderful, rounded number!)
# of authors refusing permission - 0
# of HighMag visits - 7,350
# of countries with HighMag visitors - 30 (US, UK, and France are top 3)

On a personal note, since I've been writing HighMag, we've moved across the country to our new home, my husband finished his PhD in Accounting and started a faculty position (no postdoc required...what an idea!), and my daughter has gone from being a little baby to a running, dancing toddler. HighMag has allowed me to geek out over biology, stay current with research, and get in touch with some of the top biologists in the world. All this while being a new parent and navigating a new career path in science writing. I know many of us are in (or have been in) tricky parts of our lives where balance seems a lofty goal, so I thank you for sharing this experience with me.

If you'd like to help HighMag celebrate, consider contributing your best image! As always, suggestions on making the blog better are always welcome. Email me at highmagblog@gmail.com.

February 14, 2011

Cancer cells are smart little guys, unfortunately. Many cancer therapies target a specific type of cancer cell migration, but many cancer cells are able to switch to a different mode of migration and evade the attack. Today’s image is from a paper looking at these two modes of migration by using 3D cultures of malignant breast cancer cells.

Malignant cancer cells are able to spread beyond the initial tumor, and their migration can occur from using either of two types of cancer cell migration—mesenchymal and amoeboid. Mesenchymal migration is characterized by elongated cancer cells that can undergo proteolysis of and adhesion to the extracellular matrix on which it is migrating. Cancer cells undergoing amoeboid migration are rounded and squeeze through extracellular spaces without proteolysis of or adhesion to the matrix. A recent paper looks at the distinct roles of two different adhesion adaptor proteins – paxillin and Hic-5 – in these two modes of migration. Images above are of breast cancer cells (green) grown in two different types of 3D cultures (top and bottom). Compared with the mixed morphologies of control breast cancer cells (left images), cells without paxillin (middle images) had elongated, mesenchymal morphologies. Breast cancer cells without Hic-5 (right images) had more rounded, amoeboid morphologies.

Deakin, N., & Turner, C. (2010). Distinct roles for paxillin and Hic-5 in regulating breast cancer cell morphology, invasion, and metastasis Molecular Biology of the Cell, 22 (3), 327-341 DOI: 10.1091/mbc.E10-09-0790

February 10, 2011

There are times when you finish reading a paper and you push it in front of your labmates and ask, “Did you seeeeee this?!” Hopefully, your labmates will indulge you as you do an interpretive dance explaining the coolness of the paper. If I were still in a lab, the images and paper in today’s post would be thrust in front of my labmates….great results and killer microscopy!

Focal adhesions are cellular structures that connect a cell to the underlying extracellular matrix, and play important roles in cell migration, cytoskeletal regulation, and signaling. The complex protein composition and dynamics within focal adhesions have made it difficult to understand their precise architecture. A recent paper uses a new technique called iPALM to determine the nanoscale organization of focal adhesions. This technique allowed for super-resolution images of focal adhesion components, with the added bonus of data indicating the exact depth of each component. From this data, Kanchanawong and colleagues were able to build a precise three-dimensional model of focal adhesion organization. Images above show the localization of integrin and actin using iPALM, with color-coding indicating the depth of each protein relative to the plasma membrane of the cell. When looking at a side view of the focal adhesion (bottom images), the yellow coding of integrin reveals that it resides closely to the plasma membrane on the coverglass (indicated by 0), while actin was found deeper in the cell.

Adapted by permission from Macmillan Publishers Ltd, copyright 2010.

Kanchanawong, P., Shtengel, G., Pasapera, A., Ramko, E., Davidson, M., Hess, H., & Waterman, C. (2010). Nanoscale architecture of integrin-based cell adhesions Nature, 468 (7323), 580-584 DOI: 10.1038/nature09621

February 7, 2011

Cancer is not a disease…it is many many diseases. Some cancers come about gradually, while others can occur from a single catastrophic cellular event, according to a recent paper.

Most cancers are believed to progress through a series of genetic changes that gradually allows cells to become cancerous and spread. These genetic changes are random, but can be pushed along by carcinogens or DNA repair problems. Sometimes, though, there can be big pulses of genetic change that encourage cancer progression, and a recent paper describes how single catastrophic cellular events can cause major genomic rearrangements that quickly lead to cancer. In this paper, Stephens and colleagues found multiple cancer samples with tens to hundreds of genomic rearrangements that were caused by a single catastrophic event, and termed this phenomenon “chromothripsis.” Evidence of chromothripsis can be found in at least 2-3% of all cancers, including many subtypes, and in about 25% of bone cancers. Images above show chromosomes from a renal cancer cell line, with chromosome 5 marked with different fluorescent probes that find specific genomic regions. Compared to the normal chromosome 5, the derivative chromosome 5 has gross rearrangements suggesting chromothripsis, as seen by the close juxtaposition of all of the fluorescent probes.

Stephens, P., Greenman, C., Fu, B., Yang, F., Bignell, G., Mudie, L., Pleasance, E., Lau, K., Beare, D., & Stebbings, L. (2011). Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development Cell, 144 (1), 27-40 DOI: 10.1016/j.cell.2010.11.055
©2011 Elsevier Ltd. All rights reserved.

February 3, 2011

Stereocilia are tiny structures that provide us each with the amazing ability to hear sounds. Next time you are at your favorite band’s concert, be nice to your stereocilia and stand far away from the speakers.

Stereocilia are long actin-based structures that are responsible for receiving auditory signals in our inner ears and translating them into electrical signals that our brain will understand. The actin motor myosin XVa and its cargo protein whirlin are important in stereocilia elongation, and a recent paper identifies an additional member of this complex. Eps8 is an actin-regulatory protein that interacts with myosin XVa and whirlin, and serves as a key regulator of stereocilia length. Images above show stereocilia in normal mice and mice deficient in Eps8, myosin XVa, or whirlin (top to bottom).

Copyright ©2011 Elsevier Ltd. All rights reserved.

Manor, U., Disanza, A., Grati, M., Andrade, L., Lin, H., Di Fiore, P., Scita, G., & Kachar, B. (2011). Regulation of Stereocilia Length by Myosin XVa and Whirlin Depends on the Actin-Regulatory Protein Eps8 Current Biology, 21 (2), 167-172 DOI: 10.1016/j.cub.2010.12.046