Resistance to white rust in pak choi and Chinese cabbage at the cotyledon stage

The biothrofic pathogen Albugo candida (Pers.) attacks all the cultivated Brassica species and several wild crucifers causing the disease known as white rust. The symptoms consist on the initial appearance of more or less conspicuous white sori on the plant leaves and stems, followed by severe distortions of the affected organs, especially flowers and siliqua. On delicate vegetable types of Brassica rapa L., like pak choi (B. rapa var. chinensis L.) and chinese cabbages (B. rapa var. pekinensis L.) even a slight white rust infection can render all the production unmarketable. Development of resistant cultivars is the best way to control the disease and to insure low pesticide spraying and residues in vegetables. The objective of this work were: i) the screening of a collection of B. rapa accessions from several seed banks for sources of resistance to white rust; and ii) the study of the inheritance of resistance in the most resistant accessions. Forty three accessions of B. rapa chinensis and 19 accessions of B. rapapekinensis were screened at the cotyledon stage following the methods of Santos and Dias (2004) with a Portuguese A. candida isolate Ac506 (Br) collected from turnip leaves. Four accessions of B. rapa chinensis presented more than 50% of resistant plants: the pak choi (BRA 117) was the most resistant accession with 85% of resistant plants, followed by pak choi (BRA227) with 73%, pai tsai 'Ex China 1' (B00083) with 60% and pak choi 'Ai Jiao Huang' (BRA 225) with 53%. On the opposite, B. rapa pekinensis accessions were all consider as susceptible presenting only 0-11% of resistant plants. The inheritance of resistance was studied in two crosses between pak choi BRA 117 and the rapid cycling B. rapa plant line CrGC 1.19. Selfed parents and F1 and F2 generations were produced, and screened at the cotyledon stage as previously described. Analysis of the results suggests that inheritance of resistance to Ac506 in pak choi BRA 117 is controlled by two nuclear genes with dominant recessive interaction.