Xiaoen Huang

Area of research

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Research interest

Research topics from publications: Citrus Huanglongbing is a pathogen-triggered immune disease that can be mitigated with antioxidants and gibberellin; Extracellular pyridine nucleotides trigger plant systemic immunity through a lectin receptor kinase/BAK1 complex; Transgene-free genome editing of vegetatively propagated and perennial plant species in the T0 generation via a co-editing strategy; Rhomboid-mediated cleavage of the immune receptor XA21 protects grain set and male fertility in rice; Highly efficient generation of canker resistant sweet orange enabled by an improved CRISPR/Cas9 system; Base editors for citrus gene editing; REF1 peptides significantly enhance transformation efficiency but inhibit shoot regeneration in citrus Agrobacterium -mediated transformation. Representative work: Huanglongbing (HLB) is a devastating disease of citrus, caused by the phloem-colonizing bacterium Candidatus Liberibacter asiaticus (CLas). Here, we present evidence that HLB is an immune-mediated disease. We show that CLas infection of Citrus sinensis stimulates systemic and chronic immune responses in phloem tissue, including callose deposition, production of reactive oxygen species (ROS) such as H2O2, and induction of immunity-related genes. The infection also upregulates genes encoding ROS-producing NADPH oxidases, and downregulates antioxidant enzyme genes, supporting that CLas causes oxidative stress. CLas-triggered ROS production localizes in phloem-enriched bark tissue and is followe Systemic acquired resistance (SAR) is a long-lasting broad-spectrum plant immunity induced by mobile signals produced in the local leaves where the initial infection occurs. Although multiple structurally unrelated signals have been proposed, the mechanisms responsible for perception of these signals in the systemic leaves are unknown. Here, we show that exogenously applied nicotinamide adenine dinucleotide (NAD+) moves systemically and induces systemic immunity. We demonstrate that the lectin receptor kinase (LecRK), LecRK-VI.2, is a potential receptor for extracellular NAD+ (eNAD+) and NAD+ phosphate (eNADP+) and plays a central role in biological induction of SAR. LecRK-VI.2 constitutivel