Combating citrus greening disease by simultaneously targeting the pathogen and callose-mediated phloem occlusion

Huanglongbing (HLB), caused by Candidatus Liberibacter asiaticus (CLas), disrupts sugar transport in citrus due to bacterial proliferation and excessive callose deposition that blocks sieve elements. Unblocking phloem may reduce symptoms, but it is unclear whether targeting CLas or suppressing callose deposition is more critical, as both contribute to phloem dysfunction. This study evaluated whether an integrated strategy targeting both CLas and callose-mediated phloem blockage could more effectively restore phloem transport, carbohydrate allocation, and productivity in HLB-affected citrus. Two complementary field experiments assessed the effects of an antibiotic, a callose inhibitor, and their combination on phloem recovery and source-sink dynamics. The first experiment focused on treatment-induced changes in carbon transport between source and sink shortly after delivery via stem infiltration, capturing immediate physiological responses. The second experiment assessed cumulative carbon allocation to determine sustained effects on assimilate transport and fruit development. Callose inhibitor treatment increased sugar transport but this immediate response did not yield lasting benefits. Antibiotic treatment enhanced carbon import into developing fruits, but these effects were not consistently supported by other physiological indicators. In contrast, the combined treatment reduced callose deposition, improved phloem conductivity and carbon allocation during high sink demand, decreased fruit abscission, and increased the total carbon accumulated in the fruits after physiological fruit drop. Collectively, these results demonstrate that impaired source-sink balance in HLB-affected citrus results from the combination of both pathogen load and host callose accumulation, supporting an integrated strategy that combines pathogen suppression with modulation of host phloem function to improve orchard productivity.