Floral organ development is fundamental to sexual reproduction in angiosperms. Many key floral regulators (most of which are transcription factors) have been identified and shown to modulate floral meristem determinacy and floral organ identity, but not much is known about the regulation of floral organ growth, which is a critical process by which organs to achieve appropriate morphologies and fulfill their functions. Spatial and temporal control of anisotropic cell expansion following initial cell proliferation is important for organ growth. Cortical microtubules are well known to have important roles in plant cell polar growth/expansion and have been reported to guide the growth and shape of sepals and petals. In this study, we identified two homolog proteins, QWRF1 and QWRF2, which are essential for floral organ growth and plant fertility. We found severely deformed morphologies and symmetries of various floral organs as well as a significant reduction in the seed setting rate in the qwrf1qwrf2 double mutant, although few flower development defects were seen in qwrf1 or qwrf2 single mutants. QWRF1 and QWRF2 display similar expression patterns and are both localized to microtubules in vitro and in vivo. Furthermore, we found altered cortical microtubule organization and arrangements in qwrf1qwrf2 cells, consistent with abnormal cell expansion in different floral organs, which eventually led to poor fertility. Our results suggest that QWRF1 and QWRF2 are likely microtubule-associated proteins with functional redundancy in fertility and floral organ development, which probably exert their effects via regulation of cortical microtubules and anisotropic cell expansion.

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Precise control over how and where actin filaments are created in eukaryotic cells leads to the construction of unique cytoskeletal arrays with specific functions within a common cytoplasm. Actin filament nucleators are key players in this activity and include the conserved Actin-Related Protein 2/3 (Arp2/3) complex, that creates dendritic networks of branched filaments, as well as a large family of formins that typically generate long, unbranched filaments and bundles. In some eukaryotic cells, these nucleators compete for a common pool of actin monomers and loss of one favors the activity of the other. To test whether this is a common mechanism across kingdoms, we combined the ability to image single filament dynamics in living plant epidermal cells with genetic and/or small molecule inhibitor approaches to stably or acutely disrupt nucleator activity. We found that Arp2/3 mutants or acute CK-666 treatment markedly reduced the frequency of side-branched nucleation events as well as overall actin filament abundance. We also confirmed that plant formins contributed to side-branched filament nucleation in vivo. Surprisingly, simultaneous inhibition of both nucleators increased overall actin filament abundance and enhanced the frequency of de novo nucleation events. Collectively, these observations suggest that plant cells have a unique actin filament nucleation mechanism compared to yeast or animal cells.

Summary One of the strategies that plants adopt to cope with an unfavorable environment is to sacrifice their growth for tolerance. Although moderate salt stress can induce root growth inhibition, the molecular mechanisms regulating this process have yet to be elucidated. Here, we found that overexpression of a zinc finger‐homeodomain family transcription factor, HOMEOBOX PROTEIN 24 (HB24), led to longer primary roots than in the wild‐type in the presence of 125 mM NaCl, whereas this phenotype was reversed for the hb24 loss‐of‐function mutant, indicating a negative impact of HB24 on salt‐induced root growth inhibition. We then found that salt stress triggered the degradation of HB24 via the ubiquitin–proteasome pathway, as mediated by a plant U‐box type E3 ubiquitin ligase 30 (PUB30) that directly targets HB24. We verified that HB24 is able to directly bind to the promoters of Sugars Will Eventually be Exported Transporter 11/12 (SWEET11/12) to regulate their expression in roots. Through genetic and biochemical assays, we further demonstrated that the HB24‐SWEET11 module plays a negative role in salt‐induced root growth inhibition. Therefore, we propose that under salt stress, PUB30 mediates HB24′s degradation, thereby downregulating the expression of SWEET11, resulting in reduced sucrose supply and root growth inhibition.