All raw microscopy data are on BioImage Archive and image processing tools are on GitHub. If you've seen anything like this in algae or other microbes on rich media, we'd love to hear from you. [9/9]
What triggers this? What are the wisps? Is it adaptive or a stress response? We don't know yet. We're sharing these observations now because they're unexpected and we want feedback — similar phenomena in other systems, mechanistic ideas, experimental priorities. [8/9]
We also saw reorganization of chloroplasts and mitochondria inside the transformed cells. In some, chloroplasts clustered at the periphery while mitochondria concentrated in a central zone — a striking spatial separation from their normally close association. [7/9]
When we stained with mitochondrial dyes, we detected signal within these appendages — in one case extending nearly 200 µm from the cell body. [6/9]
Some of the most striking features: thin wisp-like appendages extending from cell bodies. They were barely visible in raw images but popped out after contrast enhancement. They don't beat like flagella and seem mostly static. [5/9]
Erdschreiber's medium has similar salt levels to Marine Broth but lacks organic nutrients like peptone and yeast extract. Cells on Erdschreiber's got bigger and rounder, but didn't develop the extreme amorphous shapes. This suggests it's not just osmotic stress — organic nutrients seem key. [4/9]
The results were way more dramatic than expected. After 40+ days on Marine Broth agar, cells were way larger, amorphous, packed with vacuole-like structures, and completely non-motile. Nothing like the tidy ellipsoids you see in standard freshwater media. [3/9]
We'd previously noticed C. smithii could grow on marine media while C. reinhardtii couldn't, and that the cells looked "larger and rounded." But we'd resuspended those cells in water, which could cause osmotic swelling. So we went back and imaged them properly — in the growth medium itself. [2/9]
New pub from @ArcadiaScience 🧵 We found that C. smithii — a freshwater green alga — undergoes wild morphological transformations when grown on Marine Broth. Huge cells with mysterious wisp-like appendages. Here's what we saw. thestacks.org/publications... [1/9]
zoogle.arcadiascience.com told us Chlamy is a great model for ADA1 — so we tried it!
Come chat about it:
Sunday Dec 7, 2:15–3:45 pm (digital poster, near the @ascbiology.bsky.social booth)
Monday Dec 8, 2:15–3:45 pm (paper poster, B538)
Excited to share some new work from @arcadiascience.com at #CellBio2025!
We’re using Chlamydomonas reinhardtii as a rapid in vivo platform to model ADA1 deficiency and test computationally designed therapeutic ADA1 variants.
Poster PDF: bit.ly/chlamy-ADA
This work highlights why genetic background matters in model organisms! Even after multiple rounds of backcrossing, unexpected phenotypes can emerge that may not be directly related to the gene you're studying. @ArcadiaScience [9/9]
To figure this out, we're testing another CPC1 mutant (cpc1-2) from a different genetic background and trying to rescue both with wild-type CPC1 expression. This should tell us if these growth phenotypes are due to the mutation or genetic background. [8/9]
Why does cpc1-1 behave so differently? It might be retaining genetic material from its parent strain despite backcrossing. Or maybe the CPC1 protein itself plays a role in metabolism - it does interact with enolase and other glycolytic enzymes! [7/9]
Third, after 47 days, cpc1-1 was the ONLY strain that could grow on marine medium with high salt content, revealing an unexpected halotolerance. [6/9]
Second, on nitrate-containing media, wild-type C. reinhardtii and ida4 showed chlorosis (yellowing) as expected due to their nit2 mutation. But cpc1-1 maintained dark green colonies, suggesting it can use nitrate efficiently. [5/9]
First, cpc1-1 showed enhanced growth on media with proteose peptone, outperforming wild-type strains that barely grew in this condition! [4/9]
The cpc1-1 mutant (which has defects in the central pair complex of flagella) showed three surprising growth phenotypes that weren't present in other strains, including the ida4 mutant (which has inner dynein arm defects). [3/9]
We were studying flagellar mutants as models for human ciliary diseases when we noticed something odd about their growth patterns. So we decided to compare growth across different media types to see if these mutations affect metabolism beyond just flagellar function. [2/9]
Discovered some unexpected growth phenotypes in Chlamydomonas flagellar mutants! The cpc1-1 strain (with central pair complex defects) shows surprising metabolic traits that might be independent of its flagellar defects. 🧵 research.arcadiascience.com/pub/observat... [1/9]
Happy Darwin Day! Today, we’re thinking about how to use evolution to accelerate biomedical research. We think the answer is to expand the repertoire of organismal models. Search for the best ones using our new portal, Zoogle: zoogle.arcadiascience.com 🧵
Today at #CellBio24, I'll discuss our new pub at the "Quantitative Biology in Emerging Model Systems" subgroup session at 5:15 pm in Ballroom 20A. Come check it out!
Today at #CellBio24, Dave Mets will be at poster B599 talking about mapping genotypes to phenotypes!
poster: zenodo.org/records/1449...
Our new pub dropped this weekend!
For those at #CellBio24, I'll be at poster B73 starting at 11:15 am discussing this work!
I'll also be giving a talk on Tuesday at 5:15 pm in Ballroom 20A in the Quantitative Biology in Emerging Model Systems session
poster here: zenodo.org/records/14481493
Thanks to the team at @arcadiascience.bsky.social! Especially @taraeb.bsky.social, Ryan Lane, Dave Mets, @meganhoch.bsky.social, & Audrey Bell who made this work possible! Check out the pub here (research.arcadiascience.com/pub/result-chlamy-spgf) & feel free to comment! We love feedback! [8/8]
While this project is now on ice (explained in pub), all code & data are available: 🔗 GitHub: (github.com/Arcadia-Scie...) 📊 BioImage Archive: (www.ebi.ac.uk/biostudies/b...). [7/8]
The different effects of each drug highlight how similar swimming problems can arise from distinct molecular pathways. What works for one genetic variant may not work for another [6/8]
Despite similar motility defects, the mutations responded differently to treatment —- what rescued one mutation often had no effect on the other. This suggests mutation-specific therapeutic approaches are needed [5/8]
We developed two complementary approaches to measure motility: a population "sink-or-swim" assay and detailed single-cell tracking with SwimTracker (research.arcadiascience.com/pub/resource-swimtracker-htp-swimming-assay/release/2). This revealed how drugs affect different aspects of swimming [4/8]
