Biology of callose (β-1,3-glucan) turnover at plasmodesmata - PubMed (original) (raw)

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Biology of callose (β-1,3-glucan) turnover at plasmodesmata

Raul Zavaliev et al. Protoplasma. 2011 Jan.

Abstract

The turnover of callose (β-1,3-glucan) within cell walls is an essential process affecting many developmental, physiological and stress related processes in plants. The deposition and degradation of callose at the neck region of plasmodesmata (Pd) is one of the cellular control mechanisms regulating Pd permeability during both abiotic and biotic stresses. Callose accumulation at Pd is controlled by callose synthases (CalS; EC 2.4.1.34), endogenous enzymes mediating callose synthesis, and by β-1,3-glucanases (BG; EC 3.2.1.39), hydrolytic enzymes which specifically degrade callose. Transcriptional and posttranslational regulation of some CalSs and BGs are strongly controlled by stress signaling, such as that resulting from pathogen invasion. We review the role of Pd-associated callose in the regulation of intercellular communication during developmental, physiological, and stress response processes. Special emphasis is placed on the involvement of Pd-callose in viral pathogenicity. Callose accumulation at Pd restricts virus movement in both compatible and incompatible interactions, while its degradation promotes pathogen spread. Hence, studies on mechanisms of callose turnover at Pd during viral cell-to-cell spread are of importance for our understanding of host mechanisms exploited by viruses in order to successfully spread within the infected plant.

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Conflict of interest statement

Conflict of interest The authors declare that they have no conflict of interest.

Figures

Fig. 1

Fig. 1

Stress-induced callose accumulation at plasmodesmata in leaf epidermal cells of N. benthamiana. a Confocal image showing the pattern of wound-induced callose accumulation at pit-fields in aniline blue stained tissue. Insert: double fluorescent spots of callose at individual pit-fields (dotted line marks middle lamella). Callose was stained by incubating a strip of leaf tissue in 0.1% aniline blue for 1–2 min before observation. Intact cells adjacent to cut were observed. b Callose accumulation at pit-fields quantified after transient transformation with mutant TMV. Callose was quantified 24 h post agroinfiltration (24 hpai) with either a mutant TMV (TMV_Δ_MP_Δ_CP) which replicates, but is unable to move cell-to-cell, or an empty vector as control for agroinfection. Both are compared to control with no treatment. Virus replication alone induces high accumulation of callose in wild-type (WT) plants to levels above both controls. Virus replication coupled with cell-to-cell movement in transgenic plants expressing viral movement protein (MP+) triggers callose degradation at Pd to levels similar to control without treatment. Panel b is reproduced from Guenoune-Gelbart et al. (2008)

Fig. 2

Fig. 2

A schematic model illustrating the gating of Pd during virus infection, exemplified by TMV cell-to-cell spread. Callose (black) is deposited in the cell wall at the neck region of Pd in response to viral infection, resulting in constricted Pd aperture. Viral RNA (vRNA) initiates synthesis of replicase, movement protein (MP), and coat protein (not shown). MP associates with the endoplasmic reticulum (ER). Plant defense response to virus replication leads to synthesis of pathogenesis related β-1,3-glucanase which accumulates in the ER lumen. ER associated bodies containing replicase, MP and β-1,3-glucanase are formed. The bodies traffic to plasma membrane and deliver their lumenal cargo containing β-1,3-glucanase to the cell wall. When at cell wall, β-1,3-glucanase hydrolyzes callose, allowing Pd to dilate. MP:vRNA:replicase complex diffuses in the ER-desmotubule continuum to the next cell through dilated Pd. Reproduced from Levy et al. (2007b) with modifications

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