Petra Stirnberg

Interactions between Auxin and Strigolactone in Shoot Branching Control

In Arabidopsis (Arabidopsis thaliana), the carotenoid cleavage dioxygenases MORE AXILLARY GROWTH3 (MAX3) and MAX4 act together with MAX1 to produce a strigolactone signaling molecule required for the inhibition of axillary bud outgrowth. We show that both MAX3 and MAX4 transcripts are positively auxin regulated in a manner similar to the orthologous genes from pea (Pisum sativum) and rice (Oryza sativa), supporting evolutionary conservation of this regulation in plants. This regulation is important for branching control because large auxin-related reductions in these transcripts are associated with increased axillary branching. Both transcripts are up-regulated in max mutants, and consistent with max mutants having increased auxin in the polar auxin transport stream, this feedback regulation involves auxin signaling. We suggest that both auxin and strigolactone have the capacity to modulate each others levels and distribution in a dynamic feedback loop required for the coordinated control of axillary branching.

FHY3 promotes shoot branching and stress tolerance in Arabidopsis in an AXR1‐dependent manner

The transposase-related transcription factor FAR-RED ELONGATED HYPOCOTYL3 (FHY3) promotes seedling de-etiolation in far-red light, which is perceived by phytochrome A (phyA). In this role, FHY3 indirectly mediates the nuclear import of light-activated phyA, which triggers downstream transcriptional responses. Here, we present genetic evidence for additional roles of FHY3 in plant development and growth. New fhy3 alleles were isolated as suppressors of max2-1 (more axillary branching2-1), a strigolactone-insensitive mutant characterised by highly branched shoots. Branching suppression by fhy3, in both wild-type and max2-1 backgrounds, resulted from inhibition of axillary bud outgrowth. Additional roles in axillary meristem initiation were revealed in the revoluta (rev) fhy3 double mutant, with fhy3 enhancing rev mutant defects in axillary shoot meristem formation, as well as in floral meristem maintenance. fhy3 also affected embryonic and floral patterning with low penetrance, and displayed oxidative stress-related phenotypes of retarded leaf growth and of cell death. The fhy3 phenotypes of axillary bud outgrowth suppression and of stress-induced leaf growth retardation both required the AUXIN-RESISTANT1 gene, and are independent of phyA. Consistent with the recent discovery that FHY3 regulates many Arabidopsis promoters, our results suggest much wider roles for FHY3 in growth and development, either in concert with, or beyond, light signalling.

Mutation of the cytosolic ribosomal protein-encoding RPS10B gene affects shoot meristematic function in Arabidopsis

BackgroundPlant cytosolic ribosomal proteins are encoded by small gene families. Mutants affecting these genes are often viable, but show growth and developmental defects, suggesting incomplete functional redundancy within the families. Dormancy to growth transitions, such as the activation of axillary buds in the shoot, are characterised by co-ordinated upregulation of ribosomal protein genes.ResultsA recessive mutation in RPS10B, one of three Arabidopsis genes encoding the eukaryote-specific cytoplasmic ribosomal protein S10e, was found to suppress the excessive shoot branching mutant max2-1. rps10b-1 mildly affects the formation and separation of shoot lateral organs, including the shoot axillary meristems. Axillary meristem defects are enhanced when rps10b-1 is combined with mutations in REVOLUTA, AUXIN-RESISTANT1, PINOID or another suppressor of max2-1, FAR-RED ELONGATED HYPOCOTYL3. In some of these double mutants, the maintenance of the primary shoot meristem is also affected. In contrast, mutation of ALTERED MERISTEM PROGRAMME1 suppresses the rps10b-1axillary shoot defect. Defects in both axillary shoot formation and organ separation were enhanced by combining rps10b-1 with cuc3, a mutation affecting one of three Arabidopsis NAC transcription factor genes with partially redundant roles in these processes. To assess the effect of rps10b-1 on bud activation independently from bud formation, axillary bud outgrowth on excised cauline nodes was analysed. The outgrowth rate of untreated buds was reduced only slightly by rps10b-1 in both wild-type and max2-1 backgrounds. However, rps10b-1 strongly suppressed the auxin resistant outgrowth of max2-1 buds. A developmental phenotype of rps10b-1, reduced stamen number, was complemented by the cDNA of another family member, RPS10C, under the RPS10B promoter.ConclusionsRPS10B promotes shoot branching mainly by promoting axillary shoot development. It contributes to organ boundary formation and leaf polarity, and sustains max2-1 bud outgrowth in the presence of auxin. These processes require the auxin response machinery and precise spatial distribution of auxin. The correct dosage of protein(s) involved in auxin-mediated patterning may be RPS10B-dependent. Inability of other RPS10 gene family members to maintain fully S10e levels might cause the rps10b-1 phenotype, as we found no evidence for unique functional specialisation of either RPS10B promoter or RPS10B protein.

Auxin and strigolactones in shoot branching: intimately connected?

Axillary meristems form in the axils of leaves. After an initial phase of meristematic activity during which a small axillary bud is produced, they often enter a state of suspended growth from which they may be released to form a shoot branch. This post-embryonic growth plasticity is typical of plants and allows them to adapt to changing environmental conditions. The shoot architecture of genotypically identical plants may display completely contrasting phenotypes when grown in distinct environmental niches, with one having only a primary inflorescence and many arrested axillary meristems and the other displaying higher orders of branches. In order to cease and resume growth as required, the plant must co-ordinate its intrinsic developmental programme with the responses to environmental cues. It is thought that information from the environment is integrated throughout the plant using plant hormones as long-distance signals. In the present review, we focus primarily on how two of these hormones, auxin and strigolactones, may be acting to regulate shoot branching.

pax1-1 partially suppresses gain-of-function mutations in Arabidopsis AXR3/IAA17

BackgroundThe plant hormone auxin exerts many of its effects on growth and development by controlling transcription of downstream genes. The Arabidopsis gene AXR3/IAA17 encodes a member of the Aux/IAA family of auxin responsive transcriptional repressors. Semi-dominant mutations in AXR3 result in an increased amplitude of auxin responses due to hyperstabilisation of the encoded protein. The aim of this study was to identify novel genes involved in auxin signal transduction by screening for second site mutations that modify the axr3-1 gain-of-function phenotype.ResultsWe present the isolation of the partial suppressor of axr3-1 (pax1-1) mutant, which partially suppresses almost every aspect of the axr3-1 phenotype, and that of the weaker axr3-3 allele. axr3-1 protein turnover does not appear to be altered by pax1-1. However, expression of an AXR3::GUS reporter is reduced in a pax1-1 background, suggesting that PAX1 positively regulates AXR3 transcription. The pax1-1 mutation also affects the phenotypes conferred by stabilising mutations in other Aux/IAA proteins; however, the interactions are more complex than with axr3-1.ConclusionWe propose that PAX1 influences auxin response via its effects on AXR3 expression and that it regulates other Aux/IAAs secondarily.