TY  - JOUR
AB  - Background

The multicellular green alga Volvox carteri represents an attractive model system to study various aspects of multicellularity like cellular differentiation, morphogenesis, epithelial folding and ECM biogenesis. However, functional and molecular analyses of such processes require a wide array of molecular tools for genetic engineering. So far there are only a limited number of molecular tools available in Volvox.
Results

Here, we show that the promoter of the V. carteri nitrate reductase gene (nitA) is a powerful molecular switch for induction of transgene expression. Strong expression is triggered by simply changing the nitrogen source from ammonium to nitrate. We also show that the luciferase (g-luc) gene from the marine copepod Gaussia princeps, which previously was engineered to match the codon usage of the unicellular alga Chlamydomonas reinhardtii, is a suitable reporter gene in V. carteri. Emitted light of the chemiluminescent reaction can be easily detected and quantified with a luminometer. Long-term stability of inducible expression of the chimeric nitA/g-luc transgenes after stable nuclear transformation was demonstrated by transcription analysis and bioluminescence assays.
Conclusion

Two novel molecular tools for genetic engineering of Volvox are now available: the nitrate-inducible nitA promoter of V. carteri and the codon-adapted luciferase reporter gene of G. princeps. These novel tools will be useful for future molecular research in V. carteri.
DA  - 2015
DO  - 10.1186/s12896-015-0122-3
KW  - Co-transformation
KW  - Genetic engineering
KW  - Ammonium
KW  - Gaussia princeps luciferase gene
KW  - Green algae
KW  - Heterologous expression
KW  - Inducible promoter
KW  - Nitrate reductase
KW  - Nitrogen sources
KW  - Volvocine algae
KW  - Reporter genes
KW  - Streptomyces rimosus aphVIII gene
LA  - eng
IS  - 1
PY  - 2015
SN  - 1472-6750
T2  - BMC Biotechnology
TI  - The inducible nitA promoter provides a powerful molecular switch for transgene expression in Volvox carteri
UR  - https://nbn-resolving.org/urn:nbn:de:0070-pub-27224091
Y2  - 2024-11-22T06:51:18
ER  -