Characterization and transcriptomic analysis of a novel yellow-green leaf wucai ( Brassica campestris L.) germplasm

Background Leaf color mutants are the ideal materials to explore the pathways of chlorophyll (Chl) metabolism, chloroplast development, and photosynthesis system. In this study, a spontaneous yellow-green leaf wucai ( Brassica campestris L.) mutant “WY16–13” was identified, which exhibited yellow-green leaf color during its entire growth period. However, current understanding of the molecular mechanism underlying Chl metabolism and chloroplast development of “WY16–13” is limited. Results Total Chl and carotenoid content in WY16–13 was reduced by 60.92 and 58.82%, respectively, as compared with its wild type parental line W16–13. Electron microscopic investigation revealed fewer chloroplasts per cell and looser stroma lamellae in WY16–13 than in W16–13. A comparative transcriptome profiling was performed using leaves from the yellow-green leaf type (WY16–13) and normal green-leaf type (W16–13). A total of 54.12 million (M) (WY16–13) and 56.17 M (W16–13) reads were generated. A total of 40,578 genes were identified from the mapped libraries. We identified 3882 differentially expressed genes (DEGs) in WY16–13 compared with W16–13 (i.e., 1603 upregulated genes and 2279 downregulated genes). According to the Gene Ontology (GO) term and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, these DEGs are involved in porphyrin and Chl metabolism [i.e., chlorophyllase ( CLH ), heme oxygenase ( HO ), chlorophyll (ide) b reductase ( NYC ), and protochlorophyllide oxidoreductase ( POR ) genes], carbohydrate metabolism, photosynthesis, and carbon fixation in photosynthetic organisms. Moreover, deficiency in Chl biosynthetic intermediates in WY16–13 revealed that the formation of the yellow-green phenotype was related to the disorder of heme metabolism. Conclusions Our results provide valuable insights into Chl deficiency in the yellow-green leaf mutant and a bioinformatics resource for further functional identification of key allelic genes responsible for differences in Chl content.