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

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

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

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

If you have Cancer, this is your visualization. That... is a cancerous cell reaching Apoptosis and Necrosis—they are gone. — Natural Killer (NK) cells play a the primary role in the immune system's defense against cancer. They induce cancer cell death primarily through two mechanisms: Apoptosis Necrosis Apoptosis is a programmed, non-inflammatory form of cell death, while necrosis is a more abrupt and inflammatory process. In many cases, NK cells can trigger a combination of both, leading to mixed forms of cell death. This dual capability allows NK cells to effectively target and destroy all tumor cells. Their ability to act without prior sensitization makes them vital for early cancer surveillance and curing existing cancer. One of the only ways cancer never starts or stops entirely is NK cells. They are the guerrilla warfare troops that never sleep. This is why it is vital for BioShield by to be approved, NOW for every cancer, not just a single cancer type. With the rest needing years and years of tests. Cancer is cancer, unregulated cell division and NK cells are NK cells. The ONLY thing that stops BioShield is government betrayal, and organized corruption disguised as following the “regulations” designed by the entrenched gatekeepers of corporate protection. Everyone knows it works that has even a molecule of biological understanding. Now you know.show more

A new combination technique enables DNA sequencing and high-resolution... imaging in intact cells — offering new insights into progeria and aging. Jason Buenrostro Fei Chen Lab Ajay Labade Caroline Comenho zack chiang Science Magazineshow more

Did a quick and dirty implementation of a spatial... hash structure to speedup RTAO, ray results are stored in cells indexed by pos/normal/cell size and after storing a few rays occlusion can be queried from the cell instead of raytracing it. 3x faster RTAO with no denoising.show more

Our latest preprint! Some beautiful cell biology in this... one. "Presynapses are mitophagy pit stops that prevent axon degeneration" Discoveries into the cell biology of of mitophagy in axons, a disease mechanism, and a potential therapeutic avenue. 1/2show more

Some microbes carry a protein, called SNIPE, that "chops... up" phage DNA as it's being injected into the cell. This is a new mechanism for phage defense! CRISPR–Cas and restriction enzymes also evolved to fight against phages, but they work by recognizing sequences. SNIPE works, instead, by sensing "touch." SNIPE is a protein with about 500 amino acids. After it's made by the ribosome, it latches onto ManYZ, two proteins which sit on the cell's inner membrane. (ManYZ is an importer; it brings mannose and other sugars into the cell.) Once attached to ManYZ, SNIPE sits and waits for an invading phage. Some phages, including lambda, actually infect cells by pushing their DNA through this ManYZ channel. Lambda uses its "tail" to reach inside the protein channel, basically, and inject its DNA. When this physical touch happens, though, SNIPE is waiting. As soon as the phage DNA starts entering the cell, and passes through ManYZ and SNIPE, it gets immediately destroyed. This means that SNIPE is the first phage defense system discovered, so far, that uses spatial positioning at the injection site to destroy invaders. But there are caveats, of course. If you untether SNIPE from ManYZ, such that it can freely diffuse through the cell, it will chew up the bacterium's genome. It is not a highly discerning nuclease! Also, SNIPE is not found in most bacteria. A prior pangenome study, which sequenced lots of different microbes, found that roughly a third of well-studied bacterial lineages had at least one member with a SNIPE-like protein. (For this paper, they just ported one of those homologs into an E. coli laboratory strain.) And finally, because SNIPE's mechanism is tightly tied to ManYZ, it cannot be used to defend against phages that enter the cell through different routes. T4 phages, for example, inject their DNA straight through the cell membrane and into the cytoplasm, without interacting with ManYZ. This is a nice basic science paper. Applications TBD. (Just remember that scientists figured out that bacteria had a phage defense system, called CRISPR-Cas, many years before it was repurposed into a gene-editing tool.) P.S. The video below shows how cells with the SNIPE gene (middle row) kill invading phages, and thus continue growing and dividing. Empty vector (top row) refers to bacteria carrying a plasmid with no SNIPE gene; this is a control group. And SNIPE E414A refers to cells which received a mutated SNIPE gene, where the glutamate at position 414 has been changed to an alanine, thus destroying the protein's nuclease activity. These cells also die when they get infected with a phage.show more

Jimin is a sone through and through 🥰 Hyo:... There are members who are thin right? So they order (supper) to gain weight, even if I don't say it, you're a pink blood so you know who they are right? Karina: Can I guess? Yoona unnie and Sooyoung unnie Hyo: Yeah those two were the main onesshow more