Decode the Functional Genome: Move Beyond Transcriptomic Profiling to Measure Protein Synthesis Rates.
High mRNA expression does not guarantee functional protein. In fact, transcript levels only explain ~40% of protein abundance variability. Translatomics (Translational Profiling) eliminates this blind spot by sequencing the "active" genome—the mRNAs actively bound by ribosomes.
From optimizing mRNA vaccine codons to discovering tumor neoantigens, CD Genomics provides the high-resolution data needed to decode the final, most critical layer of gene regulation. Our portfolio includes Polysome Profiling, Ribo-seq, Disome-seq, and tRNA-seq.
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Translatomics is the genome-wide analysis of mRNA molecules that are actively occupied by ribosomes. Unlike total RNA sequencing, which measures the potential for gene expression, translatomics measures the kinetic reality of protein production.
A common challenge in drug discovery is the disconnect between gene expression data and phenotypic outcomes.
While proteomics measures the steady-state accumulation of proteins (the net result of synthesis minus degradation), translatomics measures the instantaneous rate of synthesis. This makes it far more sensitive for detecting acute stress responses, drug mechanisms of action (MoA), and identifying short peptides (sORFs) often missed by mass spectrometry.
Navigating the translatome requires the right resolution for your specific research question. Use this matrix to select the optimal service.
| If your research question is... | Recommended Service | Key Output Data |
|---|---|---|
| "I need to find novel peptides/antigens for a vaccine." | Ribo-seq | Novel ORFs, uORFs, non-canonical start sites. |
| "I want to know if my drug stops global protein synthesis." | Polysome Profiling | Monosome/Polysome Ratio (Peak Map). |
| "My protein yield is low, but mRNA is high. Why?" | Disome-seq | Pause Scores, Ribosome Collision Sites. |
| "Which splice variant is actually making protein?" | Standard RNC-seq & Long-read RNC-seq | Full-length translated isoforms. |
| "I have very little sample (e.g., sorted cells)." | Enhanced Ribo-seq | High-complexity libraries from low input. |
| "I am studying mitochondrial metabolic defects." | MitoRibo-seq | Mitochondrial-specific ribosome footprints. |
Ideal for Mechanism of Action (MoA), Neoantigen Discovery, and Codon Optimization.
Ribo-seq (Ribosome Profiling) The gold standard for translatomics. We use RNase digestion to isolate ~30nt Ribosome Protected Fragments (RPFs), mapping ribosome positions with nucleotide precision.
Ideal for Protein Folding, Stress Response, and mRNA Therapeutic Design.
Disome-seq (Ribosome Collision Analysis) Standard Ribo-seq cannot distinguish between active elongation and stalling. Disome-seq specifically captures the ~60nt footprints of colliding ribosomes (disomes).
Ideal for Phenotype Screening and Translational Status Checks.
Polysome Profiling We use sucrose density gradient centrifugation to physically separate mRNA into sub-polysomal (inactive) and polysomal (active) fractions.
Ideal for Isoform Validation.
RNC-seq (Ribosome-Nascent Chain Complex Seq) Unlike Ribo-seq which digests RNA, RNC-seq sequences full-length mRNAs bound to ribosomes.
tRNA Sequencing (tRNA-seq) Quantifies the abundance and charging status of transfer RNAs. Essential for correlating codon usage bias with translational speed.
From Discovery to Clinic: Solving Pharma Challenges
The Challenge: High mRNA stability does not always equal high protein expression. "Silent" mutations can create accidental ribosome stall sites. The Solution: Use Ribo-seq and Disome-seq to map ribosome density across your construct. Identify "slow" codons or secondary structures causing bottlenecks and optimize the sequence for "smooth" translation.
The Challenge: Standard RNA-seq misses short, cryptic peptides presented by MHC-I molecules. The Solution: Ribo-seq reveals translation initiating from non-canonical start sites (e.g., CUG, GUG) in 5' UTRs or "non-coding" RNAs, identifying novel tumor-specific antigens.
The Challenge: Many compounds affect cellular phenotypes (Translational Buffering) without altering mRNA levels. The Solution: Compare Polysome-seq vs. RNA-seq to identify gene sets specifically repressed by your compound, distinguishing between transcription inhibitors and translation elongation blockers.
Technical Superiority in Translatomics
Translatomics is technically unforgiving. A slight delay in lysis or incorrect digestion can ruin the library. Here is why we are the preferred partner for complex studies.
Ribosomes are dynamic. If cells are stressed during harvest, ribosomes "run off" the mRNA.
We have optimized workflows for:
We do not just deliver raw reads. We prove the data is real.
Client: Senior Scientist, Immunology Dept, Mid-sized Biotech (Boston, MA) Project: Ribo-seq on FACS-sorted T-cells.
"We were skeptical about doing Ribo-seq because we could only isolate about 100,000 cells. Other vendors told us we needed 5 million. CD Genomics used their Enhanced Ribo-seq protocol. Not only did we get successful libraries, but the P-site mapping rate was over 85%, and we clearly saw the translational shift in our target cytokines."
Client: Principal Investigator, Neurobiology Institute (Germany) Project: Disome-seq for Neurodegenerative Disease Model.
"We had a phenotype where our mRNA levels were normal, but protein aggregates were forming. We sent flash-frozen tissue for Disome-seq. The data was pristine—we saw a distinct ~60nt fragment peak (confirming disome isolation) and identified a specific stalling motif.
| Sample Type | Recommended Amount | Handling Requirement |
|---|---|---|
| Cell Lines | > 1 × 10^7 cells | Lysis buffer with CHX immediately upon harvest. |
| Animal Tissue | > 200 mg | Snap-freeze in liquid nitrogen within seconds. |
| Plant Tissue | > 500 mg | Grind in liquid nitrogen; specialized buffer required. |