Dataset Information

ERECTA Regulates Cell Elongation by Activating Auxin Biosynthesis in Arabidopsis thaliana.

ABSTRACT: The ERECTA family genes, ERECTA (ER), ERECTA-LIKE1 (ERL1), and ERECTA-LIKE2 (ERL2), encode leucine-rich repeat receptor-like kinases in Arabidopsis thaliana. Knocking out these three genes can cause severe phenotypes, which indicates that they play significant roles in plant growth and development. However, the molecular mechanism within remains unclear. Here we show that the short hypocotyl phenotypes of er erl1 erl2 mutants are mainly due to the defects of cell elongation rather than the cell division. In contrast, in the ERECTA overexpression transgenic plants, the hypocotyl length is increased with elongated cells. Moreover, we show that the er erl1 erl2 triple mutant contains a low level of auxin, and the expression levels of the key auxin biosynthesis genes are significantly reduced. Consistent with this observation, increasing exogenous or endogenous auxin levels could partially rescue the cell elongation defects of the er erl1 erl2 triple mutant. Therefore, our results provide a molecular basis for auxin mediated ERECTA control of the hypocotyl length in Arabidopsis thaliana.

SUBMITTER: Qu X

PROVIDER: S-EPMC5623719 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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ERECTA Regulates Cell Elongation by Activating Auxin Biosynthesis in Arabidopsis thaliana.

Qu Xiaoya X Zhao Zhong Z Tian Zhaoxia Z

Frontiers in plant science 20170927

The ERECTA family genes, ERECTA (ER), ERECTA-LIKE1 (ERL1), and ERECTA-LIKE2 (ERL2), encode leucine-rich repeat receptor-like kinases in Arabidopsis thaliana. Knocking out these three genes can cause severe phenotypes, which indicates that they play significant roles in plant growth and development. However, the molecular mechanism within remains unclear. Here we show that the short hypocotyl phenotypes of er erl1 erl2 mutants are mainly due to the defects of ce ...[more]

PMID: 29021806

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Project description:Plants use shade avoidance strategy to escape the canopy shade when grown under natural conditions. Previous studies showed that the Arabidopsis receptor-like kinase ERECTA (ER) is involved in shade avoidance syndrome. However, the mechanisms of ER in modulating SAR by promoting hypocotyl elongation are unknown yet. Here, we report that ER regulated hypocotyl elongation in shade avoidance requires auxin and gibberellins (GAs). The T-DNA insertional ER mutant er-3 shows a less hypocotyl length than that in Col-0 wild type. Promoter::GUS staining analysis shows that ER and its paralogous genes ERECTA-LIKE1 (ERL1) and ERECTA-LIKE2 (ERL2) are differentially expressed in the seedlings, of which only ER is most obviously upregulated in the hypocotyl by shade treatment. Exogenous feeding assay by using media-application with vertical-grown of Arabidopsis seedlings showed that the hypocotyl length of er-3 is partially promoted by indol-3-acetic acid (IAA), while it is relatively insensitive of er-3 to various concentrations of IAA than that of Col-0. Hypocotyl elongation of er-3 is promoted similar to that of Col-0 by high temperature in the white light condition, but the elongation was not significantly affected by the treatment of the auxin transport inhibitor 1-N-naphthylphthalamic acid (NPA). Exogenous GA3 increased the hypocotyl elongation of both er-3 and the wild type in the shade condition, and the GA3 biosynthesis inhibitor paclobutrazol (PAC) severely inhibits the hypocotyl elongation of Col-0 and er-3. Further analysis showed that auxin biosynthesis inhibitors yucasin and L-kynurenine remarkably inhibited the hypocotyl elongation of er-3 while yucasin shows a more severe inhibition to er-3 than Col-0. Relative expression of genes regulating auxin homeostasis and signaling, and GA homeostasis is less in er-3 than that in Col-0. Furthermore, genetic evidences show that ER regulated hypocotyl elongation is dependent of PHYTOCHROME B (PHYB). Overall, we propose that ER regulated shade avoidance by promoting hypocotyl elongation is PHYB-dependent and requires auxin and GAs.

Project description:Background and aimsLATERAL ORGAN BOUNDARIES DOMAIN 29 (LBD29), an important molecule downstream of auxin response factors ARF7 and ARF19, has a critical role in lateral root formation in Arabidopsis thaliana. The cell cycle activation of pericycle cells and their speciﬁcation triggered by auxin are crucial for the initiation of lateral roots. In this study, we attempted to determine whether LBD29 is involved in auxin signalling and/or cell cycle regulation and to characterize the roles of LBD29 in these processes.MethodsThe impact of LBD29 on cell cycling progression in pericycle cells was investigated in lbd29 loss-of-function mutant or LBD29-over-expressing plants. The cell cycle was determined by measuring the expression of some cell cycle-related genes using in situ hybridization and quantitative real-time reverse transcription-PCR (qRT-PCR). Furthermore, the cell division in the root explants from either the lbd29 mutant, LBD29-over-expressing plants or the wild type grown in auxin-rich media was also analysed and compared by the distribution of DR5:β-glucuronidase (GUS) in the primordia or by the expression of PIN-FORMED (PIN) members and PLETHROA 1 (PLT1) which represented the auxin response by the pericycle cells.Key resultslbd29 mutation resulted in reduced numbers of lateral roots and primordia, whereas LBD29 over-expression resulted in more lateral root and primordia formation than in the wild type. More importantly, the level of LBD29 expression was found to be positively correlated with the level of expression of cell cycle-related genes and correlated with the numbers of subcellular organelles found in pericycle cells in the maturation zone. In addition, an in vitro experiment using root explants demonstrated that the presence of LBD29 was required for the maintenance of the cell division capacity of the pericycle. Furthermore, LBD29 appeared to modify PIN-dependent auxin signalling in the primordia since there was a correlated association between the expression of PINs, PLT1 and DR5:GUS and the expression of LBD29.ConclusionsThe ability of LBD29 to regulate lateral root initiation is associated with its maintenance of the cell division capacity of the pericycle in response to auxin and its involvement in the auxin signalling pathway.

Project description:BACKGROUND:Thaxtomin A (TA) is a natural cellulose biosynthesis inhibitor (CBI) synthesized by the potato common scab-causing pathogen Streptomyces scabies. Inhibition of cellulose synthesis by TA compromises cell wall organization and integrity, leading to the induction of an atypical program of cell death (PCD). These processes may facilitate S. scabies entry into plant tissues. To study the mechanisms that regulate the induction of cell death in response to inhibition of cellulose synthesis, we used Arabidopsis thaliana cell suspension cultures treated with two structurally different CBIs, TA and the herbicide isoxaben (IXB). RESULTS:The induction of cell death by TA and IXB was abrogated following pretreatment with the synthetic auxin 2,4-dichlorophenoxyacetic acid (2,4-D) and the natural auxin indole-3-acetic acid (IAA). The addition of auxin efflux inhibitors also inhibited the CBI-mediated induction of PCD. This effect may be due to intracellular accumulation of auxin. Auxin has a wide range of effects in plant cells, including a role in the control of cell wall composition and rigidity to facilitate cell elongation. Using Atomic Force Microscopy (AFM)-based force spectroscopy, we found that inhibition of cellulose synthesis by TA and IXB in suspension-cultured cells decreased cell wall stiffness to a level slightly different than that caused by auxin. However, the cell wall stiffness in cells pretreated with auxin prior to CBI treatment was equivalent to that of cells treated with auxin only. CONCLUSIONS:Addition of auxin to Arabidopsis cell suspension cultures prevented the TA- and IXB-mediated induction of cell death. Cell survival was also stimulated by inhibition of polar auxin transport during CBI-treatment. Inhibition of cellulose synthesis perturbed cell wall mechanical properties of Arabidopsis cells. Auxin treatment alone or with CBI also decreased cell wall stiffness, showing that the mechanical properties of the cell wall perturbed by CBIs were not restored by auxin. However, since auxin's effects on the cell wall stiffness apparently overrode those induced by CBIs, we suggest that auxin may limit the impact of CBIs by restoring its own transport and/or by stabilizing the plasma membrane - cell wall - cytoskeleton continuum.

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ERECTA Regulates Cell Elongation by Activating Auxin Biosynthesis in Arabidopsis thaliana.

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<i>ERECTA</i> Regulates Cell Elongation by Activating Auxin Biosynthesis in <i>Arabidopsis thaliana</i>.

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