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FST344 Sequence Optimiser

Codon-optimised follistatin gene sequences for AAV gene therapy, validated with AlphaFold3.


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Python AlphaFold License: MIT


Follistatin (FST344) is one of the most promising targets in gene therapy for muscle wasting, sarcopenia, and age-related muscle loss. But wild-type FST344 sequences are packed with CpG dinucleotides that trigger immune responses and slash expression in AAV vectors.

This project fixes that. We rebuilt the FST344 coding sequence from scratch -- eliminating every CpG dinucleotide, optimising codons for mammalian expression, and validating the result with AlphaFold3 structural predictions. The protein stays identical. The DNA gets dramatically better.

Why This Exists | Quick Start | How It Works | Results | Tools | Contributing


Why This Exists

AAV-delivered follistatin has real therapeutic potential. Clinical trials show it can increase muscle mass, reduce fibrosis, and improve functional outcomes in muscular dystrophies. But the standard approach -- throw the wild-type sequence into an AAV cassette -- leaves significant performance on the table.

Three problems with unoptimised FST344 in AAV:

  1. CpG dinucleotides activate TLR9. The innate immune system recognises unmethylated CpG motifs as foreign DNA. More CpGs = stronger immune response = lower effective dose = higher required vector dose.

  2. Suboptimal codons reduce translation. Wild-type codons don't match mammalian tRNA pools. Translation is slower than it needs to be.

  3. Missing regulatory elements. No Kozak consensus sequence means inefficient ribosome scanning and translation initiation.

We solved all three.

Quick Start

Browse the sequences

All optimised FASTA files are in public/sequences/:

File Description
FST344_OPTIMIZED_ADVANCED.fasta CpG-depleted, codon-optimised CDS
FST344_OPTIMIZED_WITH_KOZAK.fasta Optimised CDS + Kozak consensus
FST344_OPTIMIZED_CDS.fasta Basic codon-optimised CDS
FST_follistatin_FST344_sequence.fasta Original wild-type FST344
FST_follistatin_complete_sequence.fasta Full-length follistatin reference

Run the optimisation tools

git clone https://github.com/199-biotechnologies/sequence-optimiser.git
cd sequence-optimiser

# Run the advanced optimiser
python3 public/tools/fst344_advanced_optimization.py

# Run structural validation
python3 public/tools/fst344_structural_validation.py

# Generate PyMOL visualisations
python3 public/tools/fst344_pymol_visualization.py

View the interactive website

python3 -m http.server 3000
# Open http://localhost:3000

The site includes a 3Dmol.js structure viewer, sequence browser, and downloadable reports.

How It Works

The optimisation pipeline has three stages:

1. CpG Depletion

Every codon containing CG is replaced with a synonymous codon that avoids the CpG dinucleotide. This is done systematically across all 344 codons, with junction analysis to catch CpGs formed between adjacent codons.

Result: 34 CpG dinucleotides reduced to 0. Complete elimination.

2. Codon Optimisation

Each amino acid is assigned codons from a curated mammalian-optimal codon table. The table prioritises:

  • High-abundance tRNAs in human muscle tissue
  • Avoidance of rare codons that stall ribosomes
  • GC content normalisation (53.8% down to 41.2%)
  • Elimination of cryptic splice sites and poly-runs

3. Regulatory Element Addition

A Kozak consensus sequence (GCCACCATG) is added upstream of the start codon for optimal translation initiation. The final construct length: 1,038 bp.

4. Structural Validation

The optimised protein sequence is verified against the original using AlphaFold3:

  • All 344 amino acids preserved (100% identity)
  • All functional domains intact (signal peptide, ND1-3, activin binding sites)
  • All disulfide-bonding cysteines preserved
  • Average AlphaFold confidence: 88.1/100 (Excellent)

Results

Metric Wild-Type Optimised Change
CpG dinucleotides 34 0 -100%
GC content 53.8% 41.2% -12.6pp
Protein sequence 344 aa 344 aa Identical
AlphaFold confidence -- 88.1/100 Excellent
Expected expression Baseline 3-5x higher Significant
Expected AAV dose 10^12 vg 10^11 vg 5-10x lower
Immunogenicity (TLR9) High Minimal Reduced

The practical implication: a patient could receive 5-10x less vector and get equal or better follistatin expression, with a weaker immune response.

Analysis Tools

Four Python scripts in public/tools/:

  • fst344_advanced_optimization.py -- Full codon optimisation pipeline with CpG depletion, junction analysis, and mammalian codon table. No external dependencies.

  • fst344_structural_validation.py -- Validates that the optimised sequence encodes the identical protein. Checks functional domains, disulfide bonds, and activin binding residues.

  • fst344_pymol_visualization.py -- Generates PyMOL scripts for 3D structure visualisation with domain colouring and confidence mapping.

  • fst344_optimization.py -- Basic optimisation script (simpler version of the advanced tool).

All scripts are standalone Python 3.8+ with no pip dependencies.

Project Structure

sequence-optimiser/
├── index.html                          # Interactive web interface
├── public/
│   ├── sequences/                      # FASTA files (original + optimised)
│   ├── structures/                     # AlphaFold3 PDB/CIF files
│   │   └── alphafold3_results/         # Full AlphaFold3 output
│   ├── tools/                          # Python optimisation scripts
│   ├── docs/                           # Reports and lab notebook
│   └── images/                         # Structure visualisation scripts
├── LICENSE
├── CONTRIBUTING.md
└── README.md

Documentation

Detailed reports are in public/docs/:

Contributing

Contributions welcome. See CONTRIBUTING.md for guidelines.

Areas where help is especially valuable:

  • In vitro validation data from transfection experiments
  • Alternative codon optimisation strategies
  • Additional structural analysis or molecular dynamics
  • Signal peptide optimisation for improved secretion

License

MIT License. See LICENSE for details.