Our goal for this project was to genetically modify an organism to produce chocolate compounds in order to combat the climate and labor issues related with chocolate production. When we originally researched the pathways needed to create these compounds, we were debating between choosing E. coli or Saccharomyces cerevisiae, as many of the papers we read had successfully created these compounds in those species.
However, we ended up choosing Lactococcus lactis cremoris (CCUG 21954, ATCC 9625, NCTC 7019, LMG 7932, IFO 3427) as the host organism when we found that one of our compounds could be produced in L. lactis, specifically 4-Hydroxy-2,5-dimethyl-3(2H)-furanone (HDMF) (Hayashida et al. 2001). Furthermore, we chose L. lactis because it has a long-standing reputation for being food-safe, producing many of the dairy products we enjoy such as cheese, butter, and buttermilk (Madera et al. 2003). Additionally, the pathways for the production of other chocolate compounds documented in E. coli had common precursors presumed to also be present in L. lactis (Xu et al. 2020).
We chose our plasmid, pNZ8148, because nisin, which induces our promoter, is also commonly used in the food industry (Zhang et al. 2024). Nisin is a broad-spectrum bacteriocin produced by L. lactis used extensively as a food preservative (O’Reilly et al. 2023). The combination of pNZ8148 and the use of L. lactis, on top of the purification of our compound, would ensure that our product would pose a lower risk to human consumption.
We created four pathways for the production of four chocolate compounds: 2-Phenylethylamine, theobromine, 4-Hydroxy-2,5-dimethyl-3 (2H)-furanone (HDMF) (also known as the trademark name Furaneol), and 3-ethyl-2,5-dimethylpyrazine. Each coding region is preceded by a ribosome binding site (either BBa_B0032 or BBa_J34801), which is further preceded by the inducible nisin promoter (BBa_K4307009). Downstream of the coding region is the terminator found inside of the original pNZ8148 plasmid (Accession CP068658.2, Region 399302 - 399354).
Even though there’s only one PDC pathway, we had three different amino acid sequences which all coded for PDC from three different organisms: PDC from Psychroflexus gondwanensis, Psychroflexus torquis, and Solanum lycopersicum.
In addition to these pathways, the nisin signal transduction pathway found in our nisin promoter is as follows:
We successfully assembled our vectors inside of pNZ8148. We did this through HiFi assembly. We first designed primers specific to each pathway which would amplify pNZ8148 with a 5’ overhang homologous to the 5’ end of the coding region. For example, for the TDH-KBL pathway (Fig. 5) a reverse primer would have homology with the 5’ end of the TDH coding region and a forward primer would have homology with the 5’ end of the KBL coding region (see Fig. 7).
This 20 base pair overhang is crucial for HiFi assembly. 3 enzymes constitute HiFi assembly: 5’ exonuclease, DNA polymerase, and DNA ligase. 5’ exonuclease chews back more of the 5’ end strand to create a longer overhang so that the two fragments anneal together, DNA polymerase fills in the gaps, and DNA ligase seals any nicks and covalently links the DNA fragments together.
In order to prepare the PCR products for HiFi assembly for higher efficiencies, two additional steps were taken: DpnI to digest methylated DNA, and column purification to further purify our DNA.
Once the plasmid was constructed, we first cloned the plasmid inside of E. coli. Then, we could extract the plasmid and transform it into our final host organism, L. lactis. Only then could we induce the plasmid by adding nisin to the media and start producing our chocolate compounds.
Unfortunately, we had many issues with cloning, both in E. coli and L. lactis.
We first tried cloning inside of DH5a E. coli cells. While each gene construct ended up growing up on an LB + chloramphenicol plate (Fig. 8), when we performed colony PCR, hardly any colonies were positive for our gene insert (Fig. 9).
We had successful insertion and cloning of gene #2 (five out of seven with a positive result), gene #3 (one out of seven), and #4 (one out of seven). However, we also learned that our plasmid required cloning inside of recA+ strains of E. coli, and DH5a competent cells lack the recA protein. The lack of recA results in plasmid instability and the potential deletion of the chloramphenicol resistance gene (NICE Expression Handbook and Volff et al. 1997). Therefore, we moved all future cloning attempts to be strictly inside of MC1061 cells.
The colony PCRs show significant improvement of MC1061 compared to DH5a. While DH5a resulted in 0/45 colonies, MC1061 had positive results in every single lane (excluding the mishap on the left gel in Fig. 11 (c)). All of our positive colony PCR results in this latest round came from MC1061, indicating plasmid stability inside of MC1061.
However, cloning inside of MC1061 was far from perfect. Despite attempting transformation six different times, only one attempt resulted in colonies that grew. This highlights our underlying issues with the replication of our plasmid inside of E. coli. After growing liquid cultures from the one successful attempt and purifying that plasmid, we attempted transformation into L. lactis. Unfortunately, nothing grew.
In addition to realizing the lack of plasmid stability in the DH5a recA- strain, there was an underlying issue with the overall replication and viability of our plasmid in both E. coli and L. lactis. After contacting NovoPro labs, the supplier of our plasmid, we determined that there was a mutation within the repC region. NovoPro labs conducted three generations of full-length sequencing on the pNZ8148 to find the mutation. This could be one of the major reasons why we’ve been having a lot of trouble cloning inside of both E. coli and L. lactis. They have since sent us a plasmid with the fixed repC region, and we plan to repeat many of our experiments with the fixed plasmid.
Going back to square one, we started on using re-building our construct with the fixed plasmid. We took this time to address many of our previous issues as well. Firstly, we designed new primers that would add BioBrick assembly prefixes and suffixes in order to make them BioBrick compatible. We also designed primers to address removing the DXMT enzyme (see the note in Fig. 3). Finally, we added a pathway for the expression of EGFP in order to characterize both the strength of our promoter (we would see EGFP expression at varying concentrations of nisin) and to check for any unwanted promoter expression when it is not being induced, as it is possible that our promoter is not fully repressed in E. coli (NICE Expression Handbook).