ARS | Publication request: Callose deposition and inhibited symplastic transport in the phloem of citrus leaves infected with Candidatus Liberibacter asiaticus

Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: June 17, 2011
Publication Date: August 28, 2011
Citation: Koh, E., Zhou, L., Kang, B., Williams, D.S., Duan, Y. 2011. Callose deposition and inhibited symplastic transport in the phloem of citrus leaves infected with Candidatus Liberibacter asiaticus. Plant Physiology. DOI: 10.1007/s00709-011-0312-3.

Technical Abstract: Huanglongbing (HLB) is a lethal disease of citrus, damaging citrus agriculture worldwide. A phloem-limited, alpha proteobacterium, Candidatus Liberibacter asiaticus (Las) is associated with HLB in North America. We examined Lasinfected (Las+) leaf phloem cells by microscopy methods to characterize plant responses to Las infection and their relation to HLB pathogenecity. Citrus trees at early stage of infection display blotchy yellowing of leaves. The leaf yellowing is caused by excessive starch accumulation in the chloroplasts that limits stroma space for thylakoid membrane. Leaves from Las+ citrus plants retained 14C radioactivity longer after 14CO2 pulse labeling than leaves from uninfected citrus plants did, suggesting that starch accumulation in the Las+ leaves is due to slow export of photosynthates. In the Las+ leaf phloem cells, plasmodesmata (PD) and sieve plates were stained with a callose-specific dye and the callose deposition preceded starch over-accumulation. When phloem PD were examined by transmission electron microscopy, PD with abnormally large callose deposits were more abundant in the Las+ samples than in the uninfected samples. Las infection induced callose formation at the sieve plate that reduces sizes of sieve pores. We also demonstrated that symplastic transport of a fluorescent dye is impaired in Las+ leaves. Our results indicate that Las infection accompanies callose synthesis around PD and sieve pores of leaf phloem cells and suggest that defective phloem transport due to abnormal callose formation contribute to development of HLB symptoms.