Enhanced Carotenoid Production in Chlamydomonas reinhardtii by Overexpression of Endogenousand Exogenous Beta-Carotene Ketolase ( BKT ) Genes
is a unicellular green alga that can grow heterotrophically by using acetate as a carbon source. Carotenoids are natural pigments with biological activity and color, which have functions such as antioxidant, anti-inflammatory, vision protection, etc., and have high commercial value and prospects. We...
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Veröffentlicht in: | International journal of molecular sciences 2023-07, Vol.24 (14), p.11382 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | is a unicellular green alga that can grow heterotrophically by using acetate as a carbon source. Carotenoids are natural pigments with biological activity and color, which have functions such as antioxidant, anti-inflammatory, vision protection, etc., and have high commercial value and prospects. We transformed
with the
genes from
(
) and Chlamydomonas reinhardtii (
) via plasmid vector, and screened out the stable transformed algal strains C18 and P1. Under the condition that the cell density of growth was not affected, the total carotenoid content of C18 and P1 was 2.13-fold and 2.20-fold higher than that of the WT, respectively.
increased the levels of β-carotene and astaxanthin by 1.84-fold and 1.21-fold, respectively, while
increased them by 1.11-fold and 1.27-fold, respectively. Transcriptome and metabolome analysis of C18 and P1 showed that the overexpression of
only up-regulated the transcription level of
and
(the gene of lycopene e-cyclase). However, in P1, overexpression of
also led to the up-regulation of
(the gene of ζ-carotene desaturase) and
(the gene of β-carotene hydroxylase). Metabolome results showed that the relative content of canthaxanthin, an intermediate metabolite of astaxanthin synthesis in C18 and P1, decreased. The overall results indicate that there is a structural difference between
and
, and overexpression of
in
seems to cause more genes in carotenoid pathway metabolism to be up-regulated. |
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ISSN: | 1422-0067 1661-6596 1422-0067 |
DOI: | 10.3390/ijms241411382 |