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 of
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,
- Award ID(s):
- 1923589
- PAR ID:
- 10479188
- Publisher / Repository:
- WILEY
- Date Published:
- Journal Name:
- The Plant Journal
- Volume:
- 116
- Issue:
- 3
- ISSN:
- 0960-7412
- Page Range / eLocation ID:
- 756 to 772
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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SUMMARY KRP2 promotes trichome branching and endoreduplication which is similar tokak loss of function mutants. KAK directly interacts with KRP2 and mediates KRP2 degradation. Mutation ofKAK results in the accumulation of steady‐state KRP2. Consistently, inkak pKRP2:KRP2‐GFP plants, 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. -
Summary Mitogen‐activated protein kinase (
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Abstract Brassinosteroids (
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Abstract The TTG2 transcription factor of
Arabidopsis regulates a set of epidermal traits, including the differentiation of leaf trichomes, flavonoid pigment production in cells of the inner testa (or seed coat) layer and mucilage production in specialized cells of the outer testa layer. Despite the fact that TTG2 has been known for over twenty years as an important regulator of multiple developmental pathways, little has been discovered about the downstream mechanisms by which TTG2 co-regulates these epidermal features. In this study, we present evidence of phosphoinositide lipid signaling as a mechanism for the regulation of TTG2-dependent epidermal pathways. Overexpression of theAtPLC1 gene rescues the trichome and seed coat phenotypes of thettg2-1 mutant plant. Moreover, in the case of seed coat color rescue,AtPLC1 overexpression restored expression of the TTG2 flavonoid pathway target genes,TT12 andTT13/AHA10 . Consistent with these observations, a dominantAtPLC1 T-DNA insertion allele (plc1-1D) promotes trichome development in both wild-type andttg2-3 plants. Also,AtPLC1 promoter:GUS analysis shows expression in trichomes and this expression appears dependent on TTG2. Taken together, the discovery of a genetic interaction betweenTTG2 andAtPLC1 suggests a role for phosphoinositide signaling in the regulation of trichome development, flavonoid pigment biosynthesis and the differentiation of mucilage-producing cells of the seed coat. This finding provides new avenues for future research at the intersection of the TTG2-dependent developmental pathways and the numerous molecular and cellular phenomena influenced by phospholipid signaling. -
Abstract 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.