Reward to our Followers: From May 1st, everyone who follows @SunBiotech on Twitter/X will be able to enjoy 15% OFF for one gene-editing strain! The discount is valid for 3 months. Thank you to all our followers for your trust! Contact📧[email protected]

Most CRISPR worm strains start the same way: a glass needle aimed at a worm about 1 mm long. Need injections for your project? 📩 [email protected] The mix goes into the gonad, where developing eggs take it up. A few days later, the next generation shows whether the edit or transgene worked. Knock-ins, knock-outs, extrachromosomal arrays, single-copy insertions: all of them begin here. You design the gene. We hold the needle. Tell us the gene you wish you could edit, and we will help plan it.

A genetic test report says “variant of uncertain significance.” Nobody knows yet what it does. Could a worm help? Have a human variant to test? 📩 [email protected] Over 7,600 C. elegans genes have human counterparts. With CRISPR, we can write the exact patient change into the worm gene and watch what happens: cilia, movement, lifespan, a fluorescent reporter. In a 2022 study, 8 uncertain TMEM67 variants were knocked into worm mks-3. The worm assays flagged 5 as pathogenic-like and 3 as benign-like. Send us your gene and variant, and we will help plan the strain.

Can you watch two proteins meet inside a living worm? With split Venus BiFC (VN/VC), yes. Planning an interaction study? 📩 [email protected] What is BiFC? Split Venus (VN/VC) is a fluorescent protein cut into two halves. Fuse one half to each protein you study, and the worm lights up only where the two proteins come together. What it can show: whether two proteins meet in a living animal, and in which cells, tissues or subcellular compartments. With inducible expression, it can also show when. Send us your thoughts, and we will help plan the constructs.

Today's Nobel Prize in Medicine honors optogenetics — and C. elegans was among the first animals ever controlled with light. Planning an optogenetics project? 📩 [email protected] Laureate Georg Nagel was first author of the 2005 study that switched on channelrhodopsin-2 in worm neurons with blue light and triggered behavior (Nagel et al., Curr Biol 2005). One practical detail: worms need all-trans retinal on the plate for the channel to work. We build the cell-specific strains — tell us your neuron or tissue and we'll help you plan it.

SunyBiotech marks 10 years of service to the C. elegans community, with a special 10th-anniversary promotion for returning clients and new collaborators alike. For details, or any question about C. elegans, please write to us: 📩 [email protected] To our valued clients, thank you for 10 years of trust. To researchers who have not yet worked with us, we extend a warm welcome and invite you to be part of this milestone.

One mutation, and a worm lives twice as long as normal. Have an aging-pathway project in mind? 📩 [email protected] In 1993, Cynthia Kenyon's lab found that a single mutation in daf-2 — the C. elegans insulin/IGF-1 receptor — nearly doubles lifespan (Kenyon et al., Nature 1993). The effect depends entirely on daf-16, a FOXO transcription factor: remove daf-16, and the extra lifespan disappears. Studying this pathway usually means precise daf-2 alleles, tissue-specific daf-16 rescue, or a daf-16::GFP nuclear-translocation reporter to watch the pathway switch on and off. That's the kind of strain we build — tell us your allele or reporter design and we'll help you plan it.

The gene-silencing technique that won a Nobel Prize started with worms simply eating bacteria carrying double-stranded RNA (Fire & Mello, Nature 1998 → Nobel Prize 2006). Have a project in mind? 📩 [email protected] RNAi silences a gene temporarily — a CRISPR knock-in changes it permanently, in exactly the cells you choose. If your gene resists RNAi, or you need a stable line instead of a fading knockdown, that's what we build. Tell us your gene and target tissue and we'll help you plan it. I put the email right after the hook this time (around character 220), so it should be visible in the feed preview without anyone tapping "Show more" — while the fuller RNAi-vs-CRISPR explanation after it gives people who do expand a real reason to keep reading, rather than just a fact-and-email.

This worm turns green when its mitochondria are stressed — hsp-6p::GFP lights up the moment mitochondrial protein folding breaks down. Want this reporter for your own gene or other mitochondria projects? Email your project: 📩 [email protected]

unc-119 mutants barely crawl. Insert your construct with a working unc-119, and only correctly edited worms move normally again — a built-in screen you can read on a plain scope, no PCR needed. 📩 [email protected]

Dpy-10 co-CRISPR trick After a CRISPR injection, most F1 worms didn't take up your edit — and you can't tell which ones did just by looking.Co-inject a repair template for dpy-10 along with your real gene edit. Worms that also took it up show up as Roller or Dumpy under the scope — no PCR needed to spot them — and they're enriched for carrying your actual edit too (Arribere et al., Genetics 2014). 📩 [email protected] — send us your gene and let's talk strategy.

Summer's winding down, and in most C. elegans labs that means one thing: a wave of new rotation students, new hires, and grant-year projects about to start — all needing strains that don't exist yet. Here's the timing mistake we see every fall: a project gets scoped for an incoming student, but the strain request doesn't go out until the student actually arrives. CRISPR knock-in generation — guide design, microinjection, F1/F2 screening, and homozygosing a clean line — is measured in weeks, not days, even for a straightforward edit. The fix costs nothing and takes five minutes: send us the gene and edit as soon as the project is scoped, before the start date is even locked in. That way day one is spent collecting data, not waiting on genotyping. Got a fall project taking shape? Send us your gene and desired edit and we'll give you a realistic delivery window: [email protected]

Need to knock down a protein in just one tissue, at just the right time? You've got two very different tools for that — and picking wrong costs you weeks. Auxin-inducible degradation (AID): tag your protein, drive TIR1 in the tissue you care about, then add auxin whenever you want the knockdown to start. ~80% of target protein is gone within 30 min, near-complete by 60 min (Martinez et al., G3 2020) — real pharmacological on/off control, reversible by removing auxin. ZIF-1/ZF1 degron: tag your protein with ZF1, drive ZIF-1 in your tissue of interest. Degradation is just as fast (~20–30 min half-life), but ZIF-1 is naturally active during early embryogenesis — so a ZF1-tagged protein gets degraded there too, regardless of your tissue-specific promoter (Armenti et al., Development 2014). If your protein of interest is already GFP-tagged, a GFP-nanobody::ZIF-1 toolkit sidesteps that problem entirely (Wang et al., Development 2017). If you needed a knockdown you could switch on with a drug at exactly the right developmental stage, which would you reach for — AID, or ZIF-1? And why? Planning a conditional knockdown? Send us your gene, target tissue, and stage — we'll help you weigh AID vs ZIF-1/ZF1: [email protected]

C. elegans sperm don't swim. They crawl — using a single pseudopod, no tail, no flagellum, and not even the actin-and-myosin machinery that powers crawling in virtually every other cell type. The motor is Major Sperm Protein (MSP), which self-assembles into filaments that push the pseudopod forward at roughly 20–30 μm/min. Unlike actin, MSP doesn't even bind ATP directly — it's an entirely separate, independently evolved cytoskeletal motility system doing the same basic job actin does everywhere else in biology. Not the kind of thing that shows up in a general biology textbook, but a genuinely distinct model system for studying cell crawling and cytoskeletal dynamics. Working on cytoskeletal dynamics, motility, or reproduction in C. elegans? We'd be glad to talk through strain design for it: [email protected] #Celegans #CellBiology #WormTwitter

Healthy mitochondria turn this dye red. Failing ones leave it green — and in C. elegans, you can watch that shift happen in a live, moving animal. JC-1 is a cationic dye that accumulates in mitochondria based on membrane potential: in healthy, polarized mitochondria it forms red-fluorescing J-aggregates; in depolarized ones it stays as green monomers (Reers et al., Biochemistry 1991). The red:green ratio tracks membrane potential independent of mitochondrial size or density. MitoTracker Red works on the same potential-dependent accumulation principle, for simpler single-channel imaging. Why measure this at all: mitochondrial membrane potential naturally declines with age in C. elegans, and experimentally restoring it is enough to extend lifespan (Berry et al., Nature Aging 2023). A dye plus a fluorescence microscope gives a direct, quantifiable readout of mitochondrial health — no transgenic reporter required. C. elegans is well suited to this kind of imaging: a transparent body for live in-situ visualization, self-fertilizing hermaphrodites that keep genetic background uniform, and a ~2–3 week lifespan that makes aging and stress-response experiments fast (Brenner, Genetics 1974). We run Mitochondria Analysis with MitoTracker Red or JC-1 — staining, fluorescence imaging, and intensity quantification. Send us your strain and condition of interest: [email protected] #Celegans #Mitochondria #WormTwitter

A standard multicopy GFP reporter in C. elegans is silenced in the germline almost 100% of the time — described as "almost fully penetrant" silencing (Al Johani et al., 2020, Nat Commun). That's not a corner case, it's the default. The cause: high-copy, repetitive injected DNA is targeted by the germline's piRNA/small-RNA surveillance and shut down — regardless of whether the gene it's reporting is actually on or off. If you're comparing expression across conditions or genotypes with an array reporter, some of what you're measuring may be silencing, not real biology. A single-copy CRISPR knock-in at the endogenous locus sidesteps this: native promoter, introns, and 3'UTR stay intact, so it reads out true expression pattern and level changes — germline included. Vicencio et al. (2019, Genetics) demonstrated exactly this with "Nested CRISPR," built from off-the-shelf ssDNA/PCR reagents. Tracking expression across a mutant, a stress condition, or a time course? Send us the gene and where you need the tag (N-terminal, C-terminal, or a transcriptional reporter) — we'll help you pick the strategy: [email protected] #Celegans #CRISPR #WormTwitter

BioID's enzyme (BirA*) needs ~37°C to work well. C. elegans lives at 15–25°C — which kept proximity labeling out of worm labs for years. TurboID fixed that: it stays highly active down to ~22°C, finally letting researchers use it in flies and worms (Branon et al., 2018, Nat Biotechnol). A 2021 J Biol Chem study used a single-copy CRISPR knock-in to fuse TurboID to the endogenous elks-1 gene in C. elegans — just 2h of biotin at room temp revealed known plus previously uncharacterized synaptic proteins. Planning a TurboID fusion? Send us your target gene and terminus: [email protected] #Celegans #CRISPR

SunyBiotech Brochure New: A quick look at what's inside our brochure — service list, pricing, turnaround time etc all in one place. Want the full version, or a personalized quote? Email us: [email protected]

Anti-Obesity Drug Screening in C. elegans: Why the Worm Model Holds Up Obesity now affects more than 1 billion people worldwide — and it's not just a weight number, it's a metabolic disease that drives type 2 diabetes, cardiovascular disease, NAFLD, chronic kidney disease, hypertension, and more. C. elegans is one of the better whole-organism models for finding compounds that intervene here, and it's not just because it's small and fast: → Fatty acid synthesis, elongation, desaturation, and β-oxidation are conserved pathways, not just analogous ones → Insulin, serotonin, and neuropeptide signaling regulate fat storage in the worm much like they do in mammals → A genome-wide RNAi screen found 400+ genes that change body fat when knocked down — most with direct mammalian homologs It's not just theoretical: a 2022 whole-organism screen of 1,200 FDA-approved drugs in C. elegans found hit compounds that reduced fat, several of which were independently confirmed to have anti-obesity effects in mammals afterward. Our anti-obesity screening covers: → Fat semi-quantification (Oil Red O staining) → Triglyceride content determination → Fatty acid composition analysis What's the biggest bottleneck in your metabolic compound pipeline right now — hit identification, mechanism validation, or just throughput? [email protected] or DM us. #Celegans #DrugScreening #Obesity #DrugDiscovery #Metabolism

10 years, 13,000+ transgenic C. elegans lines, and one very big anniversary offer — let's start with how we got here. Since 2016: 1,400+ researchers served across 35 countries, 1,000+ active lab collaborations, and 1,100+ of our strains cited across 400+ papers — Nature, Cell, PNAS, Nature Communications, Aging Cell, and more. Labs at Harvard, MIT, UCSF, Max Planck, and the MRC have used our strains. Here's what we're doing to celebrate Two ways in, through September 30: New to SunyBiotech → 50% off your first custom strain. Bring a fellow C. elegans lab along and it goes up to 55% off — they get an exclusive discount of their own too. Already a customer → you're not an afterthought here. There's a very exclusive returning-client discount as well. Email us and we'll walk you through it. [email protected] or DM us.

Running a compound screen in C. elegans sounds simple — dose it, count survivors. What actually determines whether the data holds up is everything else around that. We run screens across all categories, eg: → Lifespan / anti-aging — full survival curves with proper censoring, not just a median lifespan number → Toxicity — acute, chronic, developmental, reproductive, and trans-generational, with dose-response curves for EC50/LC50 → Phenotype — locomotion, pharyngeal pumping, brood size, morphology, fluorescent reporters, and stress resistance (oxidative, heat, UV, cold, heavy metal, osmotic, hypoxic) Same infrastructure covers anti-aging, neurodegenerative, anti-obesity, anti-cancer, and anti-infective screening — the assay design changes, the rigor doesn't. C. elegans earns its place here: ~40–60% gene homology with humans, a full lifespan of 2–3 weeks, and a whole-organism readout instead of a single cell line's response. Phenotype-based hits translate too — one Alzheimer's model screen found a simple swim-exhaustion readout correlated well with real lifespan and healthspan improvements in its hit compounds. What eats the most time when you run screens yourself — the worm handling, the scoring, or the stats afterward? Happy to talk through your compound list — [email protected] or DM us.