Wallace Marshall
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wallaceucsf.bsky.social
Wallace Marshall
@wallaceucsf.bsky.social
professor at UCSF, engineer turned cell biologist, wants to know how cells solve geometry problems
Wow this is super interesting!!!!
November 12, 2025 at 12:23 AM
Yeah, I’ve seen videos like that - I think they are made by Stentor-haters who make a big deal out of how the Amoeba wins. But the way I see it amoeba ends up having to engulf the Stentor’s ass so I’m just not sure that’s a win.
November 12, 2025 at 12:22 AM
you make a really good point - it seems like its mostly giant cells that are good at healing wounds and regenerating, I have always thought maybe cells that are really big have enough cytoplasm that they can survive longer, which gives them time to make repairs. but that's just speculation...
November 11, 2025 at 4:47 PM
wow really? yeah I would assume so if whatever got wounded had something hard enough? maybe in testate amoebas?
November 11, 2025 at 4:46 PM
more like something from Carcass!
November 11, 2025 at 4:44 PM
this has been a wonderful collaboration between our two labs, led by Ambika Nadkarni @biochembika.bsky.social. We are grateful for funding by NIH and NSF
November 10, 2025 at 5:47 PM
the need to pump water out might not be limited to Stentor - even in humans the extracellular environment isn't always isotonic. When exercise or pathology changes the extracellular milieu, does this affect how cells like cardiac muscle heal wounds?
November 10, 2025 at 5:47 PM
our conclusion: it's not enough to heal wounds, you also have to restore cytoplasmic composition after any changes that occurred while the wound was open and stuff was bleeding out and water flowing in.
November 10, 2025 at 5:47 PM
amazingly, this worked! If syntaxin RNAi cells are cut in hypertonic media, they don’t die!
November 10, 2025 at 5:47 PM
if it is true that Syntaxin's role in wound healing is to restore cytoplasmic osmolarity, then it should be possible to suppress the post-wounding death phenotype by cutting cells in hyper-osmotic media, reducing the drive for water to enter.
November 10, 2025 at 5:47 PM
Ambika hypothesized that maybe when the cell is cut, water rushes in, and the CV is needed to pump it back out after the membrane heals. In this model, syntaxin RNAi cells die because they can't pump the water back out so the cytoplasm gets too diluted.
November 10, 2025 at 5:47 PM
while the hull was gashed, water leaked into your boat. So, you use a bilge-pump to pump the water back out. In a sense, the CV is basically a cellular bilge-pump.
November 10, 2025 at 5:47 PM
but why would a defect in contractile vacuole activity cause cells to die after wounding? That got us thinking: imagine you are in a boat and run over a rock that makes a gash in the hull. You patch it as fast as you can, but you still aren't out of the woods.
November 10, 2025 at 5:47 PM
As with other freshwater protists, Stentor has a contractile vacuole (CV) that accumulates water and then ejects it by transiently fusing with the plasma membrane. These vesicles made us think of CVs that couldn't fuse.
November 10, 2025 at 5:47 PM
by injecting fluorescent markers into the cytoplasm, Ulises Diaz was able to show that these blisters were actually huge membrane-bound vesicles docked near the cell surface.
November 10, 2025 at 5:47 PM
so what else could be going on? If you go back and look at the image of the Syntaxin RNAi cells, they often show what looks like blisters on their surface.
November 10, 2025 at 5:47 PM
but this seems not to be the case: after wounding, the RNAi cells survive for more than an hour and only start to die after least 90 minutes, which is not what we would expect if the membrane was not getting patched.
November 10, 2025 at 5:47 PM
Given the role of syntaxin in membrane fusion, and the fact that Stentor apparently heals its membrane rapidly which must somehow entail fusion of vesicles, the obvious hypothesis is that the syntaxin RNAi impairs membrane fusion
November 10, 2025 at 5:47 PM
one hit jumped out: Syntaxin. Cells with a Stentor Syntaxin ortholog knocked down showed a huge drop in survival, only ~37% cells survived (vs 98% controls)!
November 10, 2025 at 5:47 PM
Ambika Nadkarni took on the challenge of identifying molecular pathways required for wound healing. She used a candidate approach combining RNAi with a parallelized version of the Stentor cutting device to rapidly screen through a set of candidate genes
November 10, 2025 at 5:47 PM
using a microfluidic device, Tang lab student Kevin Zhang found that even when large wounds are created by chopping cells in half, the membrane closes up in about 100 seconds.

pubmed.ncbi.nlm.nih.gov/33810789/
Microfluidic guillotine reveals multiple timescales and mechanical modes of wound response in Stentor coeruleus - PubMed
While events local to the wound site have been the focus of many single-cell wound repair studies, our results suggest that large-scale mechanical behaviors may be of greater importance to single-cell wound repair than previously thought. The work here advances our understanding of the wound respons …
pubmed.ncbi.nlm.nih.gov
November 10, 2025 at 5:47 PM
For example, you can cut a huge gash and pull out most of the cytoplasm in Stentor and it will flow back in

pubmed.ncbi.nlm.nih.gov/24378633/
November 10, 2025 at 5:47 PM