Identification of autophagy gene family in potato and the role of StATG8a in salt and drought stress

Abstract Autophagy is a highly conserved method of recycling cytoplasm components in eukaryotes. It plays an important role in plant growth and development, as well as in response to biotic and abiotic stresses. Although autophagy‐related genes (ATGs) have been identified in several crop species, their particular role in potato ( Solanum tuberosum L.) remains unclear. Several transcription factors and signaling genes in the transgenic lines of the model plant Arabidopsis thaliana, such as AtTSPO, AtBES1, AtPIP2;7, AtCOST1 as well as AtATI1/2, ATG8f, GFP‐ATG8F‐HA, AtDSK2, AtNBR1, AtHKT1 play crucial functions under drought and salt stresses, respectively. In this study, a total of 29 putative StATGs from 15 different ATG subfamilies in the potato genome were identified. Their physicochemical properties, evolutionary connections, chromosomal distribution, gene duplication, protein–protein interaction network, conserved motifs, gene structure, interspecific collinearity relationship, and cis‐regulatory elements were analyzed. The results of qRT‐PCR detection of StATG expression showed that 29 StATGs were differentially expressed in potato's leaves, flowers, petiole, stem, stolon, tuber, and root. StATGs were dynamically modulated by salt and drought stresses and up‐regulated under salt and drought conditions. Our results showed that the StATG8a localized in the cytoplasm and the nucleus. Potato cultivar “ Atlantic ” overexpressing or downregulating StATG8a were constructed. Based on physiological, biochemical, and photosynthesis parameters, potato lines overexpressing StATG8a exhibited 9 times higher drought and salt tolerance compared to non‐transgenic plants. In contrast, the potato plants with knockdown expression showed a downtrend in drought and salt tolerance compared to non‐transgenic potato lines. These results could provide new insights into the function of StATG8a in salt and drought response and its possible mechanisms.