Table 1.
Enzyme | Mutant | Allele | Phenotype | Reference |
---|---|---|---|---|
GMP | cyt1-1 | Knock-out | Embryo lethal | Lukowitz et al. (2001) |
vtc1-1 | Knock-down | 30% of WT ascorbate | Conklin et al. (1996, 2000) | |
GME | gme-1 | Knock-out | Male gametophyte lethal. Growth defect, rescued by boron but not by ascorbate supplementation. | Qi et al. (2017) |
gme-2 | Knock-down | 30% of WT ascorbate | ||
GGP | vtc2-4 | Single knock-out | 20% of WT ascorbate | Lim et al. (2016) |
vtc5-2 | Single knock-out | 80% of WT ascorbate | Dowdle et al. (2007); Lim et al. (2016) | |
vtc2/vtc5 | Double knock-out | Growth arrest, rescued by ascorbate supplementation | ||
GPP | vtc4-4 | Knock-out | 65% of WT ascorbate | Torabinejad et al. (2009) |
L-GalDH | lgaldh | Not reported | 30% of WT ascorbate in antisense suppression lines | Gatzek et al. (2002) |
GLDH | gldh | Knock-out | Growth arrest, rescued by ascorbate supplementation | Pineau et al. (2008) |
Phenotype analysis shows that GGP is the first enzyme fully dedicated to ascorbate synthesis since growth arrest occurring in the vtc2/vtc5 double mutant and downstream mutants is rescued by ascorbate supplementation. Although a reduced function (knockdown mutation) of genes upstream of GGP also results in lower ascorbate concentration, the lethality occurring in knockout mutants cannot be prevented by exogenous ascorbate supplementation.