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Controlling the worldwide invasive pest Drosophila suzukii remains a challenge. One promising biological method for managing this pest is the use of larval and pupal parasitoids. Unfortunately, most of the larval parasitoids fail to successfully parasitise D. suzukii larvae in laboratory experiments due to the high immunity of the pest. So far, only the summer phenotype (summer morph) of D. suzukii has been tested for parasitisation. However, the winter phenotype (winter morph) is the dominant form of D. suzukii throughout the year in the northern hemisphere. Therefore, this study investigates the immunity during parasitisation for both phenotypes using the larval parasitoid Asobara japonica and the pupal parasitoid Trichopria drosophilae. It is the first to compare across all life stages the immunity of the winter phenotype to the summer phenotype of not only D. suzukii but also D. melanogaster. Our results indicate differences in the immunity between the two phenotypes for larvae, pupae, and adults. However, the degree and direction of these differences were inconsistent across the different life stages of D. suzukii. The findings have important implications for the integrated pest management (IPM) of D. suzukii. [ABSTRACT FROM AUTHOR]

Budding yeast cells multiply by asymmetric cell division. During this process, the cell organelles are transported by myosin motors along the actin cytoskeleton into the growing bud, and, at the same time, some organelles must be retained in the mother cell. The ordered partitioning of organelles depends on highly regulated binding of motor proteins to cargo membranes. To search for novel components involved in this process, we performed a protein fragment complementation screen using the cargo-binding domain of Myo2, the major organelle transporter in yeast, as bait and a genome-wide strain collection expressing yeast proteins as prey. One robust hit was Alo1, a poorly characterized D-arabinono-1,4-lactone oxidase located in the mitochondrial outer membrane. We found that mutants lacking Alo1 exhibited defects in mitochondrial morphology and inheritance. During oxidative stress, dysfunctional mitochondria are immobilized in the mother in wild-type cells. Intriguingly, overexpression of ALO1 restored bud-directed transport of mitochondria under these conditions. We propose that Alo1 supports the recruitment of Myo2 to mitochondria and its activity is particularly important under oxidative stress., Competing Interests: Competing interests The authors declare no competing or financial interests., (© 2025. Published by The Company of Biologists.)