Lecture — Building Genomes
This week's lecture by George Church, John Glass, and Jef Boeke covered the frontier of whole-genome design and synthesis — from JCVI's minimal cell (JCVI-syn3.0, 473 genes) through the Sc2.0 synthetic yeast chromosome project and Church lab's recoded E. coli with expanded genetic codes. The recitation by Ice Kiattisewee focused on CRISPR-based metabolic engineering, directly relevant to Füzi Poiesis's auxotrophic deletion design.
CRISPR-Based Metabolic Engineering
The recitation covered CRISPR-based metabolic engineering — using CRISPR interference (CRISPRi) and activation (CRISPRa) to modulate metabolic flux without permanent gene deletion, and CRISPR-mediated chromosomal editing for stable pathway integration. Both approaches are directly relevant to Füzi Poiesis Aim 2.
Auxotrophic deletions (ΔhisD, ΔtrpB, ΔleuB). The recitation's coverage of CRISPR-mediated chromosomal deletions maps directly to the three deletion events required for Füzi Poiesis's auxotrophic coupling. CRISPRi as an intermediate step — transcriptional silencing of hisD, trpB, and leuB before permanent deletion — provides a reversible validation layer: if silencing the gene in monoculture produces the expected auxotrophic phenotype (growth arrest without exogenous amino acid), the deletion can proceed with confidence. This reduces the risk of engineering a deletion that fails to produce the intended auxotrophy due to paralogous gene compensation.
Metabolic flux toward remediation outputs. CRISPRa upregulation of the mcjABCD operon (Strain A) and the sqr-pdo bicistronic cassette (Strain B) could increase remediation output beyond what constitutive promoter expression achieves, without increasing plasmid copy number or metabolic burden. This is an Aim 2 optimization strategy not explored in the Aim 1 computational design, where promoter strength was set to moderate expression to balance output with metabolic cost.
Bioproduction — Beta-Carotene & Lycopene
The lab this week demonstrated metabolic engineering for bioproduction: engineering E. coli to produce beta-carotene and lycopene by introducing the mevalonate pathway and carotenoid biosynthesis genes from heterologous organisms. As a global student at the SynBio USFQ Node, wet-lab access was not available for this session. The conceptual connection to Füzi Poiesis is direct.
The beta-carotene/lycopene bioproduction lab demonstrates the same design logic as Füzi Poiesis Strain B: heterologous pathway expression in E. coli for production of a compound not native to the chassis. The difference is output — carotenoids for visual detection versus SQR-mediated sulfide oxidation for environmental remediation. Both require codon optimization for E. coli K-12 expression, compatible promoter selection, and validation that the heterologous pathway doesn't create toxic metabolic bottlenecks. The MALDI-TOF and HPLC pipeline from Week 10 provides the analytical framework for confirming bioproduction at the protein level — exactly the approach planned for Füzi Poiesis Aim 2 biosafety validation at UFRO-BIOREN.
Füzi Poiesis — Design Sprint
Week 12 was the primary design sprint week for Füzi Poiesis — finalizing the computational deliverables, completing the Benchling plasmid maps, and preparing the presentation. The following work was completed or finalized during this window.
The lectures this week made one tension in Füzi Poiesis more visible: the gap between what genome-scale synthesis enables (arbitrary genetic programs, virus-resistant organisms, 473-gene minimal cells) and what is appropriate for deployment in a Lafkenche sacred lake. Building genomes is now technically feasible at scales that would have seemed impossible ten years ago. The question of what should be built — and where, and with whose consent — is the question that Füzi Poiesis tries to answer not by ignoring the power of the tools but by subordinating it to a framework of indigenous governance that precedes the technology.
George Church's recoded organism work is technically the most powerful biocontainment mechanism described this week — a cell that physically cannot be infected by natural viruses and cannot survive outside a synthetic amino acid supply. But it requires a fully recoded genome, years of engineering, and institutional infrastructure that doesn't exist in Temuco. The auxotrophic ring achieves a weaker but deployable version of the same principle — dependency on an external supply that doesn't exist in the open environment — with three gene deletions and three annotated plasmids in Benchling. That is the design constraint: not what is maximally powerful, but what is buildable, verifiable, and explainable to Lafkenche communities before any organism approaches Lake Budi.