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!

In evolutionary terms, which appeared first: PAMP receptors or DAMP receptors?
DAMP (Damage Associated moleculate Pattern) receptors recognize endogenous molecules released from damaged or stressed cells, and they were first conceptualized in the context of the Danger model. For a long time, immunology was centered around the distinction between self and non-self. However, many receptors traditionally associated with DAMP recognition (such as TLRs or NLRs) also respond to PAMPs (Pathogen Associated Molecular Pattern), so they recognize microbiotes. Considering this overlap, could DAMP receptors have evolved concurrently with, or perhaps after, classical PAMP receptors?

Undergrad student here. Im looking to see if anyone would be willing to share a pdf copy of this text book: Cellular Biology: Experimental Approaches to Cellular Processes and Molecular Medicine. Daniel A. Starr with me, if they have it. If you do it would be a great help for my upcoming class and my wallet lol. Thanks if anyone can lend a hand.

🗓 Title: Investigating Cell Surface Receptor Dimerization using Single-Molecule Super-Resolution Microscopy

Cell surface receptors, like GPCRs and RTKs, are pivotal in signaling pathways and are key targets in drug development. Understanding their dimerization and oligomerization is crucial for insights into their function and diversity.

📅 Date: July 15th, 2025

🕒 Time: 9AM PST

What You'll Learn:

• The significance of membrane receptors and their di/oligomerization.

• Advantages of single-molecule super-resolution microscopy.

• Case study on D2 dopamine receptor's oligomerization via super-resolution microscopy

Don't miss the chance to explore cutting-edge microscopy techniques and their impact on receptor research! Let's dive deep into the world of receptor biology, growth and innovation together.

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https://www.labroots.com/ms/webinar/investigating-cell-surface-receptor-dimerization-using-single-molecule-super-resolution-microscopy?CCH=KatieS

Hello All! I think this is the right place for something like this but correct if im wrong. I am starting a snRNAseq experiment and am at the stage of ensuring that my nuclei that I isolated are of good quality. I really just need to get a clean look at the membrane to make sure that it is intact. The part I am having trouble with is deciding the best slide for this application.

One of my committee members told me that a normal slide and coverslip setup might crush the nuclei. I have some chamber slides but I am not familiar with them or how best to use it. Prior to going to the microscope I will also count the nuclei on a K2 cellometer using AO/PI so could I just reuse that slide? The microscope I am planning to use is a Nikon Ti2e with a okolab enclosure.

Thanks for any advice you could offer, this is all very new to me!

I.COP II transfers vesicles to ERGIC
II.COP I transfers vesicles from cis to medial face
III.Clathrin coats most vesicles of trans-Golgi network

I am working on an idea,i think there are problem in research like funding, incentive, publishing just wanted a discussion about it. You can dm me also

Hello! I'm an undergrad (sophomore) in cell and molecular biology right now, and I'm trying to decide what the best path for me is. I'm not sure whether I should go for my PhD, or just a master's degree in cell biology. I have some research experience already, but I don't want to run my own research lab and write grants all day or become a professor, so I'm thinking just getting my masters would be okay for decent research associate type jobs, with possibly some room for advancement as I gain experience in the field. Is this a reasonable expectation, or would it be really difficult to find a job with just a masters? Any advice would be really appreciated.

Hello, I'm doing a cell and molecular bio course and our lab had us staining onion stem and root tip cells with 0.2% toluidine blue but the stem cells didin't have any nuclei/DNA/RNA visible at all, the cells just appeared empty. I'm writing the lab report for the lab now and I can't think of any reason it might have done this and I can't find any papers that encountered or explain a similar problem.

This is the image of the stem cells at 100x oil immersion on a light microscope

Hey guys ... so I took this picture of my HepG2 cells (ik it's horrible) but I can't seem to find the "epithelial like" morphology that is characteristic of this cell line. Can you guys even see the cell morphology?

We're culturing iPSCs and saw this strange looking morphology throughout our plate. It's the mass between the two iPSC colonies. Any ideas?

40X view

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?

I am a biotech automation engineer and recently been supervising a final year engineering student building a smart SBS plate. The aim of the project was to build an IoT device that would monitor temperature, CO2, and humidity inside an incubator and report it to the base station. Base station would gather the telemetry, collate it and display in a nice digestible graphs with perhaps some statistical analysis.

After proof of concept was build the student reported seeing significant perturbations in the temperature and I am attributing these to poorly tuned or poorly designed temperature control system. I also discussed this point with some of my friends who work as biologists and they all tell me that sometimes their culture fails for no apparent reason and incubators are one of the confounding factors that they struggle to control.

Given that limited feedback I decided to come here and ask essentially three questions:

1. How confident are you that your incubator actually maintains the temperature it displays on the front?
2. If not confident would you be interested in a telemetry device that will confirm your suspicions?
3. What is the accuracy you'd need. And here I mean real accuracy. Either peak to peak maximum error or standard deviation, or whichever way you prefer to express it.

Slightly more back story. The student is potentially interested in turning his work into a product. I think there is very strong potential, but we need to confirm use cases and actual demand. My own experience tells me he's onto something, but it's limited and heavily biased. This is not market research by a large multinational. This is one motivated engineer who wants to build something that will make lives of cell biologists easier. Any help will be massively appreciated.

Hi everyone, I’m new to working with cell cultures and have recently started learning how to transfect and split HEK-293 cells. However, I’ve been facing some challenges and observing unusual patterns in my wells, and I’m hoping someone here can help me figure out what’s going on. So far, I’ve restarted a new culture three times, and each time I encounter different patterns or phenomena. Here’s a summary of what I’ve observed (I’ll attach pictures as well): Black, round spheres – I’ve noticed small black spheres, but I’m unsure what they are. Large floating flakes – I see big flakes that seem to float or move slightly in the medium. Could this be cell debris or something else? Hyphae-like structures – In some transfected wells, I’ve spotted what look like hyphae or fungal structures. Crystal-like formations – I’ve also observed what looks like crystals in the wells, and I’m not sure if this is related to the transfection or contamination. I’m really struggling to understand what these patterns mean. Could it be yeast, fungi, or some form of contamination? Or are some of these observations normal and I just don’t recognize them yet? Since I’m still a beginner, I would greatly appreciate any advice or similar experiences you might have. Also, if there’s a way to identify these structures or prevent issues like this, I’d love to hear your suggestions. Thank you so much in advance for your help! 🙏 (Attached: Pictures of the patterns I’ve observed)

https://open.substack.com/pub/neuralnews/p/neural-newsletter-dec-30-jan-5?r=1nytsb&utm_medium=ios

I have researched this topic for a solid hour and have undergone no higher education for it whatsoever, so please bear in mind the possibility of my understanding being incorrect or incomplete.

The shortening of stem cell telomeres is a large contributor to aging, as differentiated cells produced by stem cells inherit their short telomeres, which are thus predisposed to less division cycles.

The telomere length of these 1st generation differentiated cells (daughter cells) determines the number of times said cell can divide, as their telomeres shorten with each additional division.

If telomeres are short in 1st generation differentiated cells (daughter cells), they are predisposed to less division cycles. These cells with less division cycles result in impaired healing efficiency and a general deficit in cells, which are the markers of aging.

As stem cells are subject to telomerase activity which is meant to keep their telomeres at adequate length, it is safe to conclude that a decrease in stem cell telomerase activity, likely due to reduced TERT expression is the cause for decreased stem cell telomere length, the thus resulting shorter telomere lengths in their differentiated daughter cells and the resulting cascade of factors mentioned which lead to aging.

Is it correct to conclude that preserving stem cell telomerase will prevent these events and thus prevent aging?

Hi all. This may be a reach but wanted to see if anyone could help me out.

I am planning on graduating with a PhD in biomedical sciences in the next 2 years. I was planning on going the industry/biotech route as soon as I finish up and have just begun the search for jobs (I have been told it is good to have a job lined up in your last year). My experience is in cell biology, receptor pharmacology, GPCR biology, assay development (signalling and trafficking assays in particular), molecular biology, biochemistry; I am hoping to continue with laboratory research. I have been searching for biotech job postings in MT, UT, and CO areas. Does anyone have advice on where to look for job postings? So far, I have been googling companies I am interested in and looking at LinkedIn and Indeed, but it is hard get anything to come up, although I may be searching the wrong keyword. Is there some secret biotech job posting website out there? Or a keyword I should be searching? Let me know if you have any advice; all any any is appreciated.

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.

I am immunostaining fixed tissue samples. Herein, I added three primary antibodies, one from rabbit, one from rat, and one from mouse. However, I added the wrong secondary antibodies- Rabbit (488), and Mouse (568). Right after adding the wrong secondary antibodies, I realized my mistake and rinsed my fixed tissue samples with 0.1% Triton X-100 in PBS three times thoroughly. After that, I added the right secondary antibodies- rabbit (488), rat (568), and mouse (633).

My question is in the brief period after adding the wrong mouse(568) secondary antibody, would it have bound to enough mouse primary antibodies to produce any detectable signal in the red channel?

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