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. 2023 Aug 31;14:1230723. doi: 10.3389/fpls.2023.1230723

Figure 1.

Figure 1

Characterization of the PRK mutant. (A) Representation of the PRK genomic locus in the Clip mutant with the ClB1 isertion (containing the paromomycin resistance gene) positioned in exon 7. (B) PCR on genomic DNA to confirm the presence of the ClB1 insertion in the PRK gene in the mutant strain (Locus PRK mutant) and the presence of the intact PRK locus (Locus CC-4533) in the reference strain. (C) Anti-PRK western blot on total soluble protein extract of CC-4533 and ΔPRK strains (100% corresponds to 12 µg of total protein). (D) Total activity of reduced PRK. Desalted crude extracts of CC-4533 and ΔPRK were reduced with 20 mM DTT prior to activity measurement. (E) Spot test in TAP and minimal (HSM) media under continuous light (25°C, 100 µmol photons m-2 s-1). The reference strain CC-4533 was used as a control. 106 cells were spotted and incubated for 7 days prior to observation. (F) Growth profile comparison between PRK and CC-4533. Cultures were inoculated at 105 cells/mL and incubated in TAP under light (25°C and 100 µmol m-2 s-1). (G) Kinetic parameters of growth for PRK and CC-4533 strains, calculated from the data in (F) Left graph: mean of the maximal growth rate (µmax), Right graph: mean of the lag phase duration. Error bars represent the standard deviation on a biological triplicate. (B, C, E, F) are one representative experiment out of 3 biological replicates.