Experiment Details
| Genotype (Ecotype) |
Allele |
Treatment |
Treatment Detail |
Mutant Type |
Phenotype |
Tissue |
Development Stage |
Detection Method |
Editing Frequency |
Editing Extent |
Mutant Effect |
PMID |
| NA | WT | No treatment | No treatment | No treatment | Normal | Leaf | Three‐leaf satge | RT-PCR and cDNA sequencing | 80.00% | High | None | 32583432 |
| NA | osppr16d | Using the CRISPR/Cas9 technique to systematically knock out OsPPR16. | Two CRISPR/Cas9 vectors were constructed, as previously described (Ma et al., 2015). Three specific target sequences for OsPPR16 were designed using CRISPR‐P (Lei et al., 2014). Target1 and Target2 we | Knockout | A striking developmental phenotype was observed in leaves of osppr16 mutants, which were pale at the early developmental stage, but normally green at later stages. Chl synthesis in osppr16 is reduced during early leaf development. | Leaf | Three‐leaf satge | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |
| NA | osppr16s | Using the CRISPR/Cas9 technique to systematically knock out OsPPR16. | Two CRISPR/Cas9 vectors were constructed, as previously described (Ma et al., 2015). Three specific target sequences for OsPPR16 were designed using CRISPR‐P (Lei et al., 2014). Target3 was cloned int | Knockout | A striking developmental phenotype was observed in leaves of osppr16 mutants, which were pale at the early developmental stage, but normally green at later stages. Chl synthesis in osppr16 is reduced during early leaf development. | Leaf | Three‐leaf satge | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |
| NA | WT | No treatment | No treatment | No treatment | Normal | Leaf | Five-leaf stage | RT-PCR and cDNA sequencing | 81.00% | High | None | 32583432 |
| NA | osppr16d | Using the CRISPR/Cas9 technique to systematically knock out OsPPR16. | Two CRISPR/Cas9 vectors were constructed, as previously described (Ma et al., 2015). Three specific target sequences for OsPPR16 were designed using CRISPR‐P (Lei et al., 2014). Target1 and Target2 we | Knockout | A striking developmental phenotype was observed in leaves of osppr16 mutants, which were pale at the early developmental stage, but normally green at later stages. Chl synthesis in osppr16 is reduced during early leaf development. | Leaf | Five-leaf stage | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |
| NA | osppr16s | Using the CRISPR/Cas9 technique to systematically knock out OsPPR16. | Two CRISPR/Cas9 vectors were constructed, as previously described (Ma et al., 2015). Three specific target sequences for OsPPR16 were designed using CRISPR‐P (Lei et al., 2014). Target3 was cloned int | Knockout | A striking developmental phenotype was observed in leaves of osppr16 mutants, which were pale at the early developmental stage, but normally green at later stages. Chl synthesis in osppr16 is reduced during early leaf development. | Leaf | Five-leaf stage | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |
| NA | WT | No treatment | No treatment | No treatment | Normal | Leaf | SRS, seed ripening stage | RT-PCR and cDNA sequencing | 86.00% | High | None | 32583432 |
| NA | osppr16d | Using the CRISPR/Cas9 technique to systematically knock out OsPPR16. | Two CRISPR/Cas9 vectors were constructed, as previously described (Ma et al., 2015). Three specific target sequences for OsPPR16 were designed using CRISPR‐P (Lei et al., 2014). Target1 and Target2 we | Knockout | A striking developmental phenotype was observed in leaves of osppr16 mutants, which were pale at the early developmental stage, but normally green at later stages. Chl synthesis in osppr16 is reduced during early leaf development. | Leaf | SRS, seed ripening stage | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |
| NA | osppr16s | Using the CRISPR/Cas9 technique to systematically knock out OsPPR16. | Two CRISPR/Cas9 vectors were constructed, as previously described (Ma et al., 2015). Three specific target sequences for OsPPR16 were designed using CRISPR‐P (Lei et al., 2014). Target3 was cloned int | Knockout | A striking developmental phenotype was observed in leaves of osppr16 mutants, which were pale at the early developmental stage, but normally green at later stages. Chl synthesis in osppr16 is reduced during early leaf development. | Leaf | SRS, seed ripening stage | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |
| NA | WT | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 82.00% | High | None | 32583432 |
| NA | line 1 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 66.00% | High | Decreased | 32583432 |
| NA | line 2 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 74.00% | High | Similar | 32583432 |
| NA | line 3 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 19.00% | Poor | Decreased | 32583432 |
| NA | line 4 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 26.00% | Low | Decreased | 32583432 |
| NA | line 5 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 13.00% | Poor | Decreased | 32583432 |
| NA | line 6 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 73.00% | High | Similar | 32583432 |
| NA | line 7 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 75.00% | High | Similar | 32583432 |
| NA | line 8 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 75.00% | High | Similar | 32583432 |
| NA | line 9 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 81.00% | High | Similar | 32583432 |
| NA | line 10 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 74.00% | High | Similar | 32583432 |
| NA | line 11 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 80.00% | High | Similar | 32583432 |
| NA | line 12 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 77.00% | High | Similar | 32583432 |
| NA | line 13 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 73.00% | High | Similar | 32583432 |
| NA | line 14 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 82.00% | High | Similar | 32583432 |
| NA | line 15 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 19.00% | Poor | Decreased | 32583432 |
| NA | line 16 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 78.00% | High | Similar | 32583432 |
| NA | line 17 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 76.00% | High | Similar | 32583432 |
| NA | line 18 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 75.00% | High | Similar | 32583432 |
| NA | line 19 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 81.00% | High | Similar | 32583432 |
| NA | line 20 | RNAi | RNA interference (RNAi) by double‐stranded RNA expression was used to knock down OsPPR16. An RNAi vector was constructed by amplifying a 275 bp fragment using Zhonghua 11 complementary DNA (cDNA) as a | Knockdown | NA | Leaf | NA | RT-PCR and cDNA sequencing | 78.00% | High | Similar | 32583432 |
| NA | Complementation 1 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 2 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 3 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 4 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 5 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 6 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 7 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 8 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 9 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 10 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 11 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 12 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 13 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 14 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 15 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 16 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 17 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 18 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | The Chl content was similar to that of the WT in all seedlings that tested positive for the complementation construct and had green leaves at the three‐leaf stage. | Leaf | NA | RT-PCR and cDNA sequencing | 100.00% | Complete | Restored | 32583432 |
| NA | Complementation 19 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | Similar to the osppr16 mutant, seedlings not containing the complementation construct were Chl deficient and displayed impaired editing of rpoB‐545. | Leaf | NA | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |
| NA | Complementation 20 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | Similar to the osppr16 mutant, seedlings not containing the complementation construct were Chl deficient and displayed impaired editing of rpoB‐545. | Leaf | NA | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |
| NA | Complementation 21 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | Similar to the osppr16 mutant, seedlings not containing the complementation construct were Chl deficient and displayed impaired editing of rpoB‐545. | Leaf | NA | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |
| NA | Complementation 22 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | Similar to the osppr16 mutant, seedlings not containing the complementation construct were Chl deficient and displayed impaired editing of rpoB‐545. | Leaf | NA | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |
| NA | Complementation 23 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | Similar to the osppr16 mutant, seedlings not containing the complementation construct were Chl deficient and displayed impaired editing of rpoB‐545. | Leaf | NA | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |
| NA | Complementation 24 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | Similar to the osppr16 mutant, seedlings not containing the complementation construct were Chl deficient and displayed impaired editing of rpoB‐545. | Leaf | NA | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |
| NA | Complementation 25 | Complementation | Genetic complementation studies were also performed to ultimately confirm that OsPPR16 was responsible for the mutant phenotype of osppr16. To this end, OsPPR16 fused to its native promoter was transf | Knockout | Similar to the osppr16 mutant, seedlings not containing the complementation construct were Chl deficient and displayed impaired editing of rpoB‐545. | Leaf | NA | RT-PCR and cDNA sequencing | 0.00% | Unedited | Absent | 32583432 |