SWEET genes and TAL effectors for disease resistance in plants: Present status and future prospects

SWEET genes encode sugar transporter proteins and often function as susceptibility (S) genes. Consequently, the recessive alleles of these SWEET genes provide resistance. This review summarizes the available literature on the molecular basis of the role of SWEET genes (as S genes) in the host and corresponding transcription activator‐like effectors (TALEs) secreted by the pathogen. The review has four major sections, which follow a brief introduction: The first part gives some details about the occurrence and evolution of SWEET genes in approximately 30 plant species; the second part gives some details about systems where (a) SWEET genes with and without TALEs and (b) TALEs without SWEET genes cause different diseases; the third part summarizes the available information about TALEs along with interfering/truncated TALEs secreted by the pathogens; this section also summarizes the available information on effector‐binding elements (EBEs) available in the promoters of either the SWEET genes or the Executor R genes; the code that is used for binding of TALEs to EBEs is also described in this section; the fourth part gives some details about the available approaches that are being used or can be used in the future for exploiting SWEET genes for developing disease‐resistant cultivars. The review concludes with a section giving conclusions and future possibilities of using SWEET genes for developing disease‐resistant cultivars using different approaches, including conventional breeding and genome editing. SWEET genes function as susceptibility genes. They are activated by binding of TAL effectors (secreted by the pathogen) following a code and can be exploited for developing resistant cultivars.