STY1 and STY2 promote the formation of apical tissues during Arabidopsis gynoecium development

Gynoecium ontogenesis in Arabidopsis is accomplished by the co-ordinated activity of genes that control patterning and the regional differentiation of tissues, and ultimately results in the formation of a basal ovary, a short style and an apical stigma. A transposon insertion in the STYLISH1 (STY1) gene results in gynoecia with aberrant style morphology, while an insertion mutation in the closely related STYLISH2 (STY2) gene has no visible effect on gynoecium development. However, sty1-1 sty2-1 double mutant plants exhibit an enhanced sty1-1 mutant phenotype and are characterized by a further reduction in the amount of stylar and stigmatic tissues and decreased proliferation of stylar xylem. These data imply that STY1 and STY2 are partially redundant and that both genes promote style and stigma formation and influence vascular development during Arabidopsis gynoecium development. Consistently, STY1 and STY2 are expressed in the apical parts of the developing gynoecium and ectopic expression of either STY1 or STY2 driven by the CaMV 35S promoter is sufficient to transform valve cells into style cells. STY1::GUS and STY2::GUS activity is detected in many other organs as well as the gynoecium, suggesting that STY1 and STY2 may have additional functions. This is supported by the sty1-1 sty2-1 double mutants producing rosette and cauline leaves with a higher degree of serration than wild-type leaves. STY1 and STY2 are members of a small gene family, and encode proteins with a RING finger-like motif. Double mutant analyses indicate that STY1 genetically interacts with SPATULA and possibly also with CRABS CLAW

A genetic approach to the identification of new components regulating development in Arabidopsis thaliana

Two new genes involved in important processes of plant development were identified in the model plant Arabidopsis thaliana. The genes were isolated from mutants generated through insertional mutagenesis based on a transposon tagging approach. The first gene, ALB3, was isolated through the identification of the mutant albino3 (alb3), displaying severe defects in pigmentation and chloroplast biogenesis. The ALB3 protein shows sequence similarity to a yeast protein, OXA1, which is required in the mitochondria for proper assembly of the cytochrome oxidase complex. As ALB3 is localised in thylakoid membranes, we suggest that the ALB3 protein acts in the assembly of thylakoid membrane protein complexes and thereby is crucial for proper chloroplast development and function. The second gene, SHI, was identified through the short internodes (shi) mutation, a dwarfing mutation conferring a phenotype similar to mutants defective in the biosynthesis of the plant hormone gibberellin (GA). However, the shi mutant is unable to elongate following treatment with exogenous GA, which indicates that shi is defective in the response to GA. The level of active GA is elevated in the shi mutant, which is the expected result of reduced feedback control of GA biosynthesis. As the shi mutant phenotype is the result of overexpression of the SHI gene, we suggest that the SHI protein is a component of the GA signalling pathway, possibly acting as a repressor of GA-induced cell elongation. Sequence similarity database searches revealed that the SHI gene belongs to a new Arabidopsis gene family comprising at least eight members (SHI, LRP1, and SRS1 to SRS6). These genes encode regulatory proteins containing a putative zinc-binding RING finger-like domain. We have cloned SRS1 and SRS2, and have shown by overexpression of these genes in transgenic Arabidopsis that their gene products might function in similar processes as SHI

A highly conserved NB-LRR encoding gene cluster effective against <it>Setosphaeria turcica </it>in sorghum

Abstract Background The fungal pathogen Setosphaeria turcica causes turcicum or northern leaf blight disease on maize, sorghum and related grasses. A prevalent foliar disease found worldwide where the two host crops, maize and sorghum are grown. The aim of the present study was to find genes controlling the host defense response to this devastating plant pathogen. A cDNA-AFLP approach was taken to identify candidate sequences, which functions were further validated via virus induced gene silencing (VIGS), and real-time PCR analysis. Phylogenetic analysis was performed to address evolutionary events. Results cDNA-AFLP analysis was run on susceptible and resistant sorghum and maize genotypes to identify resistance-related sequences. One CC-NB-LRR encoding gene GRMZM2G005347 was found among the up-regulated maize transcripts after fungal challenge. The new plant resistance gene was designated as St referring to S. turcica. Genome sequence comparison revealed that the CC-NB-LRR encoding St genes are located on chromosome 2 in maize, and on chromosome 5 in sorghum. The six St sorghum genes reside in three pairs in one locus. When the sorghum St genes were silenced via VIGS, the resistance was clearly compromised, an observation that was supported by real-time PCR. Database searches and phylogenetic analysis suggest that the St genes have a common ancestor present before the grass subfamily split 50-70 million years ago. Today, 6 genes are present in sorghum, 9 in rice and foxtail millet, respectively, 3 in maize and 4 in Brachypodium distachyon. The St gene homologs have all highly conserved sequences, and commonly reside as gene pairs in the grass genomes. Conclusions Resistance genes to S. turcica, with a CC-NB-LRR protein domain architecture, have been found in maize and sorghum. VIGS analysis revealed their importance in the surveillance to S. turcica in sorghum. The St genes are highly conserved in sorghum, rice, foxtail millet, maize and Brachypodium, suggesting an essential evolutionary function.</p

TIP, a novel host factor linking callose degradation with the cell-to-cell movement of Potato virus X

The cell-to-cell movement of Potato virus X (PVX) requires four virus-encoded proteins, the triple gene block (TGB) proteins (TGB25K, TGB12K, and TGB8K) and the coat protein. TGB12K increases the plasmodesmal size exclusion limit (SEL) and may, therefore, interact directly with components of the cell wall or with plant proteins associated with bringing about this change. A yeast two-hybrid screen using TGB12K as bait identified three TGB12K-interacting proteins (TIP1, TIP2, and TIP3). All three TIPs interacted specifically with TGB12K but not with TGB25K or TGB8K. Similarly, all three TIPs interacted with ß-1,3-glucanase, the enzyme that may regulate plasmodesmal SEL through callose degradation. Sequence analyses revealed that the TIPs encode very similar proteins and that TIP1 corresponds to the tobacco ankyrin repeat-containing protein HBP1. A TIP1::GFP fusion protein localized to the cytoplasm. Coexpression of this fusion protein with TGB12K induced cellular changes manifested as deposits of additional cytoplasm at the cell periphery. This work reports a direct link between a viral movement protein required to increase plasmodesmal SEL and a host factor that has been implicated as a key regulator of plasmodesmal SEL. We propose that the TIP