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Cell differentiation and morphogenesis are crucial for the establishment of diverse cell types and organs in multicellular organisms. Trichome cells offer an excellent paradigm for dissecting the regulatory mechanisms of plant cell differentiation and morphogenesis due to their unique growth characteristics. Here, we report the isolation of an Arabidopsis mutant,aberrantlybranchedtrichome 3–1(abt3‐1), with a reduced trichome branching phenotype. Positional cloning and molecular complementation experiments confirmed thatabt3‐1is a new mutant allele ofAuxin resistant 1(AXR1), which encodes the N‐terminal half of ubiquitin‐activating enzyme E1 and functions in auxin signaling pathway. Meanwhile, we found that transgenic plants expressing constitutively active version ofROP2(CA‐ROP2) caused a reduction of trichome branches, resembling that ofabt3‐1. ROP2 is a member of Rho GTPase of plants (ROP) family, serving as versatile signaling switches involved in a range of cellular and developmental processes. Our genetic and biochemical analyses showedAXR1genetically interacted withROP2and mediated ROP2 protein stability. The loss ofAXR1aggravated the trichome defects ofCA‐ROP2and induced the accumulation of steady‐state ROP2. Consistently, elevatedAXR1expression levels suppressedROP2expression and partially rescued trichome branching defects inCA‐ROP2plants. Together, our results presented a new mutant allele ofAXR1, uncovered the effects ofAXR1andROP2during trichome development, and revealed a pathway ofROP2‐mediated regulation of plant cell morphogenesis in Arabidopsis.

The Arabidopsis (Arabidopsis thaliana) TRANSPARENT TESTA GLABRA2 (TTG2) gene encodes a WRKY transcription factor that regulates a range of development events like trichome, seed coat, and atrichoblast formation. Loss-of-function of TTG2 was previously shown to reduce or eliminate trichome specification and branching. Here, we report the identification of an allele of TTG2, ttg2-6. In contrast to the ttg2 mutants described before, ttg2-6 displayed unique trichome phenotypes. Some ttg2-6 mutant trichomes were hyper-branched, whereas others were hypo-branched, distorted, or clustered. Further, we found that in addition to specifically activating R3 MYB transcription factor TRIPTYCHON (TRY) to modulate trichome specification, TTG2 also integrated cytoskeletal signaling to regulate trichome morphogenesis. The ttg2-6 trichomes displayed aberrant cortical microtubules (cMTs) and actin filaments (F-actin) configurations. Moreover, genetic and biochemical analyses showed that TTG2 could directly bind to the promoter and regulate the expression of BRICK1 (BRK1), which encodes a subunit of the actin nucleation promoting complex suppressor of cyclic AMP repressor (SCAR)/Wiskott–Aldrich syndrome protein family verprolin homologous protein (WAVE). Collectively, taking advantage of ttg2-6, we uncovered a function for TTG2 in facilitating cMTs and F-actin cytoskeleton-dependent trichome development, providing insight into cellular signaling events downstream of the core transcriptional regulation during trichome development in Arabidopsis.

In superrosid species, root epidermal cells differentiate into root hair cells and nonhair cells. In some superrosids, the root hair cells and nonhair cells are distributed randomly (Type I pattern), and in others, they are arranged in a position‐dependent manner (Type III pattern). The model plant Arabidopsis (Arabidopsis thaliana) adopts the Type III pattern, and the gene regulatory network (GRN) that controls this pattern has been defined. However, it is unclear whether the Type III pattern in other species is controlled by a similar GRN as in Arabidopsis, and it is not known how the different patterns evolved.

Trichome development is a fascinating model to elaborate the plant cell differentiation and growth processes. A wealth of information has pointed to the contributions of the components associated with cell cycle control and ubiquitin/26S proteasome system (UPS) to trichome morphogenesis, but how these two pathways are connected remains obscure. Here, we report that HECT‐type ubiquitin ligase KAKTUS (KAK) targets the cyclin‐dependent kinase (CDK) inhibitor KRP2 (for kip‐related protein 2) for proteasome‐dependent degradation during trichome branching in Arabidopsis. We show that over‐expression ofKRP2promotes trichome branching and endoreduplication which is similar tokakloss of function mutants. KAK directly interacts with KRP2 and mediates KRP2 degradation. Mutation ofKAKresults in the accumulation of steady‐state KRP2. Consistently, inkak pKRP2:KRP2‐GFPplants, the trichome branching is further induced compared with the single mutant. Taken together, our studies bridge the cell cycle control and UPS pathways during trichome development and underscore the importance of post‐translational control in epidermal differentiation.