MicroRNAs (miRNAs) are ∼21-nucleotide noncoding RNAs that play critical roles in regulating plant growth and development through directing the degradation of target mRNAs. Axillary meristem activity, and hence shoot branching, is influenced by a complicated network that involves phytohormones such as auxin, cytokinin, and strigolactone. GAI, RGA, and SCR (GRAS) family members take part in a variety of developmental processes, including axillary bud growth. Here, we show that the Arabidopsis thaliana microRNA171c (miR171c) acts to negatively regulate shoot branching through targeting GRAS gene family members SCARECROW-LIKE6-II (SCL6-II), SCL6-III, and SCL6-IV for cleavage. Transgenic plants overexpressing MIR171c (35Spro-MIR171c) and scl6-II scl6-III scl6-IV triple mutant plants exhibit a similar reduced shoot branching phenotype. Expression of any one of the miR171c-resistant versions of SCL6-II, SCL6-III, and SCL6-IV in 35Spro-MIR171c plants rescues the reduced shoot branching phenotype. Scl6-II scl6-III scl6-IV mutant plants exhibit pleiotropic phenotypes such as increased chlorophyll accumulation, decreased primary root elongation, and abnormal leaf and flower patterning. SCL6-II, SCL6-III, and SCL6-IV are located to the nucleus, and show transcriptional activation activity. Our results suggest that miR171c-targeted SCL6-II, SCL6-III, and SCL6-IV play an important role in the regulation of shoot branch production.

Heteroblasty refers to a phenomenon that a plant produces morphologically or functionally different lateral organs in an age‐dependent manner. In the model plant Arabidopsis thaliana, the production of trichomes (epidermal leaf hairs) on the abaxial (lower) side of leaves is a heteroblastic mark for the juvenile‐to‐adult transition. Here, we show that the heteroblastic development of abaxial trichomes is regulated by a spatiotemporally regulated complex comprising the leaf abaxial fate determinant (KAN1) and the developmental timer (miR172‐targeted AP2‐like proteins). We provide evidence that a short‐distance chromatin loop brings the downstream enhancer element into close association with the promoter elements of GL1, which encodes a MYB transcription factor essential for trichome initiation. During juvenile phase, the KAN1‐AP2 repressive complex binds to the downstream sequence of GL1 and represses its expression through chromatin looping. As plants age, the gradual reduction in AP2‐like protein levels leads to decreased amount of the KAN1‐AP2 complex, thereby licensing GL1 expression and the abaxial trichome initiation. Our results thus reveal a novel molecular mechanism by which a heteroblastic trait is governed by integrating age and leaf polarity cue in plants.

Floral initiation is a major step in the life cycle of plants, which is influenced by photoperiod, temperature, and phytohormones, such as gibberellins (GAs). It is known that GAs promote floral initiation under short-day light conditions (SDs) by regulating the floral meristem-identity gene LEAFY (LFY ) and the flowering-time gene SUPPRESSOR OF OVEREXPRESSION OF CO 1 (SOC1). We have defined the role of the auxin signaling component INDOLE-3-ACETIC ACID 7 (IAA7)/ AUXIN RESISTANT 2 (AXR2) in the regulation of flowering time in Arabidopsis thaliana. We demonstrate that the gain-of-function mutant of IAA7/AXR2, axr2-1, flowers late under SDs. The exogenous application of GAs rescued the late flowering phenotype of axr2-1 plants. The expression of the GA20 oxidase (GA20ox) genes, GA20ox1 and GA20ox2, was reduced in axr2-1 plants, and the levels of both LFY and SOC1 transcripts were reduced in axr2-1 mutants under SDs. Furthermore, the overexpression of SOC1 or LFY in axr2-1 mutants rescued the late flowering phenotype under SDs. Our results suggest that IAA7/AXR2 might act to inhibit the timing of floral transition under SDs, at least in part, by negatively regulating the expressions of the GA20ox1 and GA20ox2 genes.

Gravity-induced root curvature involves the asymmetric distribution of the phytohormone auxin. This response depends on the concerted activities of the auxin transporters such as PIN-FORMED (PIN) proteins for auxin efflux and AUXIN RESISTANT 1 (AUX1) for auxin influx. However, how the auxin gradient is established remains elusive. Here we identified a new mutant with a short root, strong auxin distribution in the lateral root cap and an impaired gravitropic response. The causal gene encoded an Arabidopsis homolog of the human unconventional prefoldin RPB5 interactor (URI). AtURI interacted with prefoldin 2 (PFD2) and PFD6, two β-type PFD members that modulate actin and tubulin patterning in roots. The auxin reporter DR5 rev : GFP showed that asymmetric auxin redistribution after gravistimulation is disordered in aturi-1 root tips. Treatment with the endomembrane protein trafficking inhibitor brefeldin A indicated that recycling of the auxin transporter PIN2 is disrupted in aturi-1 roots as well as in pfd mutants. We propose that AtURI cooperates with PFDs to recycle PIN2 and modulate auxin distribution.

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Plants undergo extended morphogenesis. The shoot apical meristem (SAM) allows for reiterative development and the formation of new structures throughout the life of the plant. Intriguingly, the SAM produces morphologically different leaves in an age-dependent manner, a phenomenon known as heteroblasty. In Arabidopsis thaliana, the SAM produces small orbicular leaves in the juvenile phase, but gives rise to large elliptical leaves in the adult phase. Previous studies have established that a developmental decline of microRNA156 (miR156) is necessary and sufficient to trigger this leaf shape switch, although the underlying mechanism is poorly understood. Here we show that the gradual increase in miR156-targeted SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) transcription factors with age promotes cell growth anisotropy in the abaxial epidermis at the base of the leaf blade, evident by the formation of elongated giant cells. Time-lapse imaging and developmental genetics further revealed that the establishment of adult leaf shape is tightly associated with the longitudinal cell expansion of giant cells, accompanied by a prolonged cell proliferation phase in their vicinity. Our results thus provide a plausible cellular mechanism for heteroblasty in Arabidopsis, and contribute to our understanding of anisotropic growth in plants.

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