Abstract
The differentiation of stomata provides a convenient model for studying pattern formation in plant tissues. Stomata formation is induced by a set of basic helix-loop-helix transcription factors and inhibited by a signal transduction pathway initiated by TOO MANY MOUTHS (TMM) and ERECTA family (ERf) receptors. The formation of a proper stomata pattern is also dependent upon the restriction of symplastic movement of basic helix-loop-helix transcription factors into neighboring cells, especially in the backgrounds where the function of the TMM/ERf signaling pathway is compromised. Here, we describe a novel mutant of KOBITO1 in Arabidopsis (Arabidopsis thaliana). The kob1-3 mutation leads to the formation of stomata clusters in the erl1 erl2 background but not in the wild type. Cell-to-cell mobility assays demonstrated an increase in intercellular protein trafficking in kob1-3, including increased diffusion of SPEECHLESS, suggesting that the formation of stomata clusters is due to an escape of cell fate-specifying factors from stomatal lineage cells. While plasmodesmatal permeability is increased in kob1-3, we did not detect drastic changes in callose accumulation at the neck regions of the plasmodesmata. Previously, KOBITO1 has been proposed to function in cellulose biosynthesis. Our data demonstrate that disruption of cellulose biosynthesis in the erl1 erl2 background does not lead to the formation of stomata clusters, indicating that cellulose biosynthesis is not a major determining factor for regulating plasmodesmatal permeability. Analysis of KOBITO1 structure suggests that it is a glycosyltransferase-like protein. KOBITO1 might be involved in a carbohydrate metabolic pathway that is essential for both cellulose biosynthesis and the regulation of plasmodesmatal permeability.
Highlights
The differentiation of stomata provides a convenient model for studying pattern formation in plant tissues
As descriptions of KOBITO1 mutant alleles such as kob1-1, kob1-2, eld1-1, eld1-2, and abi8 (Cheng et al, 2000; Pagant et al, 2002; Lertpiriyapong and Sung, 2003; Brocard-Gifford et al, 2004) highly resembled the phenotype of our mutant, we sequenced KOBITO1 and found a single C→T substitution at position 2,166 bp that results in a Ser-371→Leu-371 substitution (Fig. 1B)
Our analysis of kobito1 mutants in backgrounds having deficient signaling of the TOO MANY MOUTHS (TMM)/ERECTA family (ERf) signaling pathway shows that KOBITO1 function is required for proper stomatal patterning and for the suppression of excessive stomata differentiation
Summary
The differentiation of stomata provides a convenient model for studying pattern formation in plant tissues. The formation of a proper stomata pattern is dependent upon the restriction of symplastic movement of basic helix-loop-helix transcription factors into neighboring cells, especially in the backgrounds where the function of the TMM/ERf signaling pathway is compromised. The majority of neighboring plant cells are connected symplastically by tiny plasma membrane-lined cytoplasmic channels called plasmodesmata These channels play an essential role in intercellular communications, as they lead to the formation of symplastic domains allowing cell-to-cell trafficking of small molecules, proteins, and mRNA. The PDLPs are type I plasma membrane proteins with an extracellular DUF26 domain of unknown function Their overexpression promotes plasmodesmata closure and their downregulation results in increased plasmodesmatal permeability (Thomas et al, 2008). A mutation in the callose synthase GLUCAN SYNTHASELIKE8 (GSL8) increased plasmodesmatal permeability and produced a stomata clustering phenotype, possibly, due to transcription factor escape
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