A cell dividing into two daughter cells videoed through... a microscope. Chromosomes are labeled in pink. Technique: differential interference microscopy (DIC) and fluorescence. #CellBiologyshow more

Four cancer cells displaying continuous membrane blebbing videoed through... a DIC microscope. No, these cells are not dying. #CellBiologyshow more

A cell videoed through a microscope. DNA in the... nucleus (green) and mitochondria (purple) are shown. #CellBiologyshow more

A cell videoed through a microscope. DNA (cyan), mitochondria... (yellow), and VASP (magenta) are shown. #CellBiologyshow more

A cell videoed through a microscope. DNA in the... nucleus (green) and the powerhouses/overlords of the cell, mitochondria (purple), are shown. #CellBiologyshow more

A melanoma cancer cell videoed through a microscope. DNA... in the nucleus (yellow), mitochondria (cyan), and VASP (magenta) are shown. #CellBiologyshow more

A Golgi apparatus protein in a cell videoed through... a microscope. The Golgi is saturated to show the vesicles trafficking around the cell. #CellBiologyshow more

A cancer cell videoed through a microscope. It has... 3 nuclei (magenta). The powerhouse/overlords of the cell, mitochondria, are also shown (green). #CellBiologyshow more

Mitosis is a part of the cell cycle in... which replicated chromosomes are separated into two new nuclei. Such a division gives rise to genetically identical cells in which the total number of chromosomes is maintained [source:show more

One cell. Two new beginnings. Before a cell divides,... it first copies its DNA. Then, during mitosis, the chromosomes condense, align at the cell's center, separate toward opposite sides, and form two new nuclei. Finally, cytokinesis divides the cytoplasm, producing two genetically identical daughter cells. This microscopic process allows your body to grow, repair damaged tissue, and replace old cells, millions of times every day. Life continues because cells know when it is time to become two.show more

#FluorescenceFriday #cellbiology #bioart The actin cytoskeleton at 60 nm... resolution and 3 frames/min, and its association with early endosomes (Rab5a, green), as seen in a COS-7 cell by photoactivated nonlinear structured illumination microscopyshow more

We present oblique plane microscopy with adaptive optics (AO):... One deformable mirror corrects both the light-sheet and the fluorescence detection. Movie shows cancer cells in a zebrafish xenograft model, before and after application of AO.show more

The head of a bearded dragon embryo (50 days... old), imaged with light sheet fluorescence microscopy 🦎🔬show more

Why not show real data instead of a 2D... cartoon? Left diagonal: computationally separated 3D volume-rendered movies at 15 sec intervals for 19 minutes of chromosomes, mitochondria, and the ER in the same field of dividing pig kidney cells. Middle diagonal: overlapped color channels computationally sliced in slabs through the volume to reveal internal structure and interactions throughout mitosis. Upper right: zoomed in view in one slab, showing organelle rearrangements in the left cell from metaphase through telophase.show more

A single E. coli cell, placed on a dish,... will become 70 billion cells in just 12 hours. That’s exponential growth. But a new preprint shows that it's possible to engineer E. coli to grow linearly instead, where only one daughter cell continues dividing and the other stops. First, some context. In nature, there is a bacterium called Mycobacterium smegmatis (initially discovered in 1884 in ulcers scraped from syphilis patients.) M. smegmatis is weird because it divides asymmetrically. These cells grow only from one end, and all their cell wall biosynthesis machinery is located on that one end. So when the cell divides, one daughter gets this machinery and the other gets nothing. The daughter that gets the machinery can keep dividing immediately, but the other daughter has to remake all that machinery from scratch, so its growth is delayed. E. coli doesn’t grow like this. When it divides, it pinches in the middle and splits everything evenly. Enzymes, metabolites, and proteins get partitioned more or less randomly between the two daughters. For the new preprint, though, researchers engineered E. coli to behave more like M. smegmatis. Here is how they did it: First, they deleted a gene called cyaA, which encodes an enzyme (adenylate cyclase) that makes a molecule called cAMP. cAMP is SUPER IMPORTANT! It is a nutrient sensor that instructs E. coli to switch on genes that help it digest non-glucose carbon sources when glucose is scarce. Without cAMP, E. coli cells growing on alternative carbon sources will starve; they won’t know how to eat the food. Next, they added back a “split” version of the cyaA gene into the cells. In other words, they split the gene in two so that each half of the enzyme is made separately. Cells can only make cAMP, and thus eat non-glucose carbon sources, if these two halves come together. To facilitate that “coming together,” the researchers also fused the split cyaA proteins to sticky proteins that clump together, and to a fluorescent protein (to make it easy to track these molecules in the cell.) So now some interesting things start to happen if you grow E. coli on a growth medium lacking glucose. As the cell grows, its cyaA “halves” start clumping together into a giant ball. Inside the aggregate, the two enzyme halves come together and make cAMP. And when the cell gets big enough and divides, the clump of cyaA RANDOMLY goes to either daughter cell #1 or #2. The daughter that gets the aggregate (called PA+ in this paper) can keep dividing. The daughter that doesn’t (PA–) cannot. It still grows a few times — about four divisions — because it inherits some leftover cAMP from its mother. But after that, the metabolite is diluted away, and the cell stops growing. PA+ cells went through about 23 divisions on average before their aggregate decayed. And the population of cells, as a whole, grew linearly. This paper is cool because there are many applications where exponential growth is too unpredictable and, perhaps, unsafe. If you want to engineer bacteria to deliver drugs, clean up waste, or live in the gut, you don’t want them to double uncontrollably. This paper shows you can make them expand in a controlled, linear way. Alas, mutations could break this whole engineered system. A mutation that restores cyaA, for example, would give cells a new way to make cAMP. Mutations that make the aggregates split between daughters would break the asymmetry, too. But still, I really enjoy proof-of-concept engineering papers like this.show more

Congrats Andrew Weems and everyone involved on elucidating how... blebs help cancer cells avoid anoikis (cell death when losing attachment). Study involves 3D microscopy, and doing math on cell surfaces, courtesy of the @DanuserLab computer vision wizards.show more

Nice example of actin retrograde flow in a gigantic... lamellipodium. #cytoskeleton, #actin, #microscopy, #cell-motility, #scienceshow more

Mitochondria in a cell. What is going on? Make... a guess. Test the guess. Find joy in being wrong. Guess again......... #Science #CellBiology #FindJoyInBeingWrongshow more

After a walk, Austin Wells gets a catcher's interference... and there are two on in the firstshow more

#cellbiology #bioart The actin #cytoskeleton (green) is linked to... a variety of transmembrane proteins through alpha-actinin (magenta), with such linkages being particularly dense in membrane ruffles and filopodia. As seen at 3 frames/min for 8 min by linear and non-linear structured illumination microscopy (97 and 60 nm resolution, respectively).show more