What you see, is a PtK2 Cell culture, which I treated with Cytochalasin-D over 24h, fixated with Methanol and fluorescent coloured with Antibodys (anti-tubulin dm1a and Anti Mouse IgG Cy3) and DAPI. The pictures got fused and edited by me afterwards (Fiji/ImageJ + Gimpy).

It shows a rare mitosis deformity, instead of 2 the cell forms 3 miotic spindels and splits the DNA into 3 instead of 2. This deformity happens very rarely in every cell culture, but the cells die immediately after cytokinesis.

Cytochalasin-D is a cytotoxin, which inhibits the continuation of actin through binding to the (+)-pole. Actinfilaments play a crucial part during cytokinesis, together with Myosin 2, they form the contractile ring and string the membrane/cell into 2.

So we ended with a very rare condition, that we froze with the help of the toxin in the exact right time. Enjoy and have a chill Weekend!

Can young blood reverse aging? 🩸🧬

In a recent breakthrough, researchers combined plasma serum and bone marrow from young donors to treat aging human skin cells in the lab. The treatment significantly boosted collagen production, improved cell survival, and reversed multiple hallmarks of cellular aging. This marks the first time these results have been seen in human tissue models. By studying the molecules behind these effects, scientists hope to develop future treatments that slow or even reverse aging on a cellular level.

Again 40x Magnification, and taken with a Zeiss AXIO Observer Z1 inverted Flourescence Microscope.

You see another PtK2 Cell culture, but this time we treated them with Colcemid over 24h, fixated with Methanol and coloured with Antibodys (anti tubulin dm1a and anti Mouse IgG Cy3) and DAPI. The pictures got fused and edited by me afterwards (Fiji/ImageJ + Gimpy).

Colcemid is a cytotoxin which inhibits the polarization of Mikrotubuli. When the cell goes into mitosis, the miotic spindle is unable to form, so the cell is stuck in the metaphase.

When the cell is stuck for too long, it starts an emergency reaction, in which it forms a temporary nuclear lamina and decondensates the DNA again, so transcription can start again.

After 3-4 days the cellculture dies.

We used 0,1 µg/ml of colcemid, at this concentration, the miotic spindle doesnt form correctly and the microtubuli get damaged, but not completly degraded. At around 10 µg/ml the mikrotubuli degrade rapidly.

Full Link: https://www.ninthheaven.co/issue-2-introduction-to-cancer-biology-the-somatic-mutation-theory/

Hi im super sorry if this is messy or any misspelling i have dislexia but my question is how do cells use the chemical energy form the hydrolysis to do stuff i understand that the negative charge is were it comes form and being broken off but like how dose the cell harness it is there an organelle or something we just leaned about this in our bio course at hs so i was just curious fell free to ask some clarifying questions it may be messy lol

Hi all! This is my first time visiting this sub, and I thought you all might enjoy my silly art. My Cell Biology professor refers to the sodium-potassium pump as a "Salty Banana" as a memory device, and it inspired this little doodle. Thanks for letting me share!

During the Summer Science Academy 2025, I made this movie with another participant of the course. We used glowing bacteria to create a stop-motion animation.

What do you think is that?  Growth on a human fibroblast culture with Ham's-F12, imagen at 20X.

1.Before trypsinization 2.After trypsinization

Here is a link to the study: https://doi.org/10.1038/s41556-025-01708-8

“Abstract Many neurodevelopmental defects are linked to genes involved in housekeeping functions, such as those encoding ribosome biogenesis factors. How reductions in ribosome biogenesis can result in tissue- and developmental-specific defects remains unclear. Here we describe variants in the ribosome biogenesis factor AIRIM/C1orf109 that are primarily associated with neurodevelopmental disorders. Using human cerebral organoids in combination with proteomic, single-cell RNA sequencing and single-organoid translation analyses, we identify a previously unappreciated drop in protein production during early brain development. We find that ribosome levels decrease during neuroepithelial differentiation, making differentiating cells particularly vulnerable to perturbations in ribosome biogenesis during this time. Reduced ribosome availability more profoundly impacts the translation of specific transcripts, disrupting both survival and cell fate commitment of transitioning neuroepithelia. Enhancing mTOR activity suppresses the growth and developmental defects associated with AIRIM/C1orf109 variants. This work provides evidence for the functional importance of regulated changes in global protein synthesis capacity during cellular differentiation.”

Just trying to share some research I am reading. This study caught my attention because some of it is counterintuitive.

If anyone has any insights, feel free to let me know.

Your skin cells could become brain cells, muscle cells, or even immune cells. 🧬✨

Marie, also known as Lab Skills Academy, walks us through how scientists reprogram ordinary adult cells into iPSCs, or induced pluripotent stem cells. By adding specific genes, these cells are reset to a blank-slate state, giving them the power to become nearly any cell type in the body. This breakthrough helps researchers study diseases, test treatments, and explore personalized medicine that could shape the future of healthcare.

This project is part of IF/THEN®, an initiative of Lyda Hill Philanthropies.

I've been looking at the FormLabs "biocompatible" SLA resin and SDS pretty much says it's not actually biocompatible. However, people grow cells on plastics, e.g. SBS plates. I am also aware that SLA resin is not just a monomer. It'll have all sorts of additives. The question then becomes, what are the mechanisms of cytotoxicity? I realise this is a very broad question, but I am an engineer, not a biologist, so I need somewhere to start. This is one of the starting points.

Could AI help us create virtual human cells? 🦠

Scientists are training AI to create virtual human cells, digital models that mimic how real cells behave. These simulations can predict how a cell might respond to medication, genetic mutations, or physical damage. While live lab tests are still essential, AI-powered models could make research faster, safer, and more personalized. By reducing trial-and-error in early stages, these tools could unlock faster drug discovery and bring us closer to tailored treatments for individuals.

Hi everyone, I am a writer and molecular biologist with an interest in how an understanding of life on a molecular level has transformed our view of existence and our place in the universe. Examining the history of the molecularization of the life sciences, it is clear to me that the incredible insights scientists have gained are yet to be fully appreciated by our broader society.

Here is a snapshot of the take-home messages:

What is the Molecular Revolution in Biology?

It is to peer into the molecular level of life for the first time. We didn’t have complete and direct access to it before the 1950s, and we gained access due to technological developments. These technologies helped us to unlock another level of reality, the molecular realm. In short, they came from physics and the use of X-rays and electron microscopy to access the molecular realm (and the article explores this fascinating history too).

This irreversible change in perspective is why we should regard the molecular biology revolution alongside other scientific revolutions, such as the Darwinian and Copernican revolutions.

What were the key insights of the revolution?

The understanding that we, and all living things, are made up of the same atoms (matter) as the non-living Universe (stars, rocks, water).

That molecules (combinations of atoms) can encode information, most famously, in the form of DNA, which is universal to all of life on Earth.

That Information plays a profound role in the function and evolution of living beings, transforming our view of how life works.

That on a molecular level, the constant bombardment of molecules and atoms can be described as “the molecular storm”. The interior of cells, whether a bacterium or a human cell, is a crowded, chaotic place packed with molecules big and small.

Finally, I show that this revolution is still unfolding — and as powerful new technologies converge in the coming years, it presents not only immense opportunities for humanity but also profound existential risks.

For those already familiar with molecular biology, whether professionally or as students, I believe the subject's history is fraught with issues, many of which persist to this day. I aim to highlight these, challenging them where necessary. Importantly, this revolution was overlooked by Thomas Kuhn in his book on Scientific Revolutions; furthermore, it is often alluded to but not well defined. Here, I aim to provide a rationale for the outline of this revolution.

For those new to the subject, these articles will provide some context for the subject as a whole and therefore offer powerful motivation in your endeavours to understand it.

It is also free to read on SubStack: https://substack.com/home/post/p-169497844). It has audio narration. Subscribe if you want to learn and explore all things molecular, from the origin of life to the future of life on Earth.

Let's say you just had endosymbiosis, how does the endosymbiont propagate inside the host cell?

Does it live and divide, until the host cell divides, then some of the endosymbiont cells continue being trapped in the first host cell, while the rest of the endosymbiont cells are taken by the new cell?

Or does the endosymbiont integrates somehow with the host cell, adding to the inherited information in the cell, so that it grows from cell division like other organelles?

P.S. I do not have formal studies in biology fyi.

Here is the link to the study: https://doi.org/10.1038/s43018-025-01009-x

Paper states the following context behind their research:

"CAR-T cell therapies have revolutionized the treatment of B cell malignancies1,2 and are now showing early signs of efficacy in solid cancers3,4,5,6,7,8,9. Despite ongoing progress, many patients who receive CAR therapies fail to respond or develop resistance, highlighting a critical need to further optimize current treatments. Multiple factors may contribute to disease progression following CAR treatment, which can be categorized as tumor-intrinsic, tumor microenvironment or lymphocyte-intrinsic resistance mechanisms10. Among these, factors associated with CAR-expressing lymphocytes are of particular interest because they are potentially modifiable during ex vivo cell manufacturing. Across clinical studies, the in vivo expansion and persistence of CAR-T cells is frequently associated with superior outcomes11,12,13,14,15. Recent clinical data indicates that this holds true not only for CAR-T cells but also CAR-modified NK cells (CAR-NK)16, a lymphocyte subset with desirable features for allogeneic applications17. Thus, enhancing the survivability of CAR-T and CAR-NK cells remains a major goal in the cell therapy field.

Genome-wide18,19 and focused20,21,22 CRISPR screens have recently identified FAS as a major determinant of antitumor T cell persistence under chronic antigen stimulation conditions. FAS is one of five tumor necrosis factor (TNF) superfamily death receptors that induces caspase-dependent apoptosis following engagement with an extracellular ligand23. These findings provide a strong rationale for disabling FAS signaling in receptor engineered T cells19,20,21,24,25,26,27,28; however, while the role of FAS in regulating naturally occurring T cell homeostasis is well established, whether this pathway governs CAR-T and CAR-NK longevity remains unknown. Moreover, the dominant cellular sources of FAS-L in patients with cancer remain incompletely defined. Here, we aimed to address three critical gaps in knowledge regarding the immunobiology of FAS in the context of CAR-based therapies. First, we sought to define which cells express FASLG in patients. Second, we sought to establish whether CAR-engineered lymphocyte persistence is negatively self-regulated by FASLG. Finally, we sought to determine whether FASLG is required for on-target CAR-T and CAR-NK effector functions against B cell malignancies. Our findings reveal that CAR-engineered lymphocyte persistence is governed by a FAS-L/FAS autoregulatory circuit. Thus, disruption of FAS signaling can serve as a generalizable strategy to enhance the therapeutic potency of genetically engineered T cells and NK cells."

https://open.substack.com/pub/neuralnews/p/neural-newsletter-dec-2-dec-9?utm_campaign=post&utm_medium=web

Hi there,

Here are some videos on cell biology which you may find useful. The content is at a basic level but should help people understand basic concepts in a way that's easy to understand.

RNA Transcription - https://youtu.be/erB0H4-cUyE

What is RNA? | RNA Structure and Function - https://youtu.be/_EvR1WnS4fs

What is DNA? | DNA Structure and Function - https://youtu.be/PNVmAyBAnXs

What is the Nucleus? | Nucleus Structure and Function - https://youtu.be/wfv2RH0Dqck

What are Mitochondria? | Mitochondria Structure and Function - https://youtu.be/esiGZwWSOZw

What are Stem Cells? | Hematopoeisis Explained - https://youtu.be/CB-k0BIZUAI

Feel free to leave any suggestions for future content and I shall share it here for others to benefit.

Came here to ask a question which has puzzled me for ages.

New Scientist has an article about human cells citing the work of Hayflick and Moorhead stating that (in culture) human cells will divide only 55 times due to the accumulation of telomere shortening. So, does this mean that if a single cell divides into two, the two copies are not entirely identical? I ask this because, if they were entirely identical, then presumably they'd both carry the same countdown clock and they, and all subsequent generations, would die/enter senescence simultaneosly?

Interested to know more!

We found some dark spots in our hiPSC culture. Our PI thinks that it's protein aggregation from months old penicillin/streptomycin, but it could also be something alive. I included a 10X, 20X, and 40X view. The cells are in mTESR+ media with 100X P/S.

We're gonna run analysis on it, but what do you guys think? Any ideas?

https://biochemblog.vercel.app/blog/cellorganelles

Hi guys, I'm an high school student and made a blog post for an overview of the cell organelles present in the animal cell.

Please tell me what you think :)

Hello there!

My name is Artemis! I am a student at Michigan State University, majoring in microbiology. I am hoping to be an embryologist. For my college writing class, we are doing a research project where I am required to complete and interview on someone who works in microbiology and gather information to learn more about my field. This would be a 20-30 minute video interview and can be completed anytime between now and March 11th. Although this is for a class, I would really like to learn more about my future field, so this is also for my own mind and future. I appreciate your time, feel free to reach out asking for more details! I will happily provide them and the list of questions I will ask in said interview when they are ready. Thanks again!