Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1054223 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27276461_1.fastq.gz | Fastqsanger.gz | |||
| SRR27276461_2.fastq.gz | Fastqsanger.gz | |||
| SRR27276462_1.fastq.gz | Fastqsanger.gz | |||
| SRR27276462_2.fastq.gz | Fastqsanger.gz | |||
| SRR27276463_1.fastq.gz | Fastqsanger.gz |
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Project description:Plant growth relies on the activity of key transcription factors. Here, we uncover a mechanism for organ-specific growth driven by opposing electrochemical signals that propagate in a cell-type-specific manner. Using a genetically encoded pH sensor and a pH-sensitive dye, we show that apoplastic pH in epidermal cells oscillates antiphasically relative to phloem pH. The clock component CCA1 lowers apoplastic pH in hypocotyl epidermal cells while increasing it in companion cells. This opposing regulation promotes hypocotyl growth but inhibits root elongation. Mechanistically, CCA1 activates auxin signaling in shoots while repressing SUCROSE TRANSPORTER 2 and the electrogenic (H+)-pump ATPase AHA3 by directly binding their promoters. The repression decreases sucrose loading into the phloem and slows transport velocity. Expressing CCA1 in the phloem is sufficient to inhibit root elongation, whereas AHA3 over-expression in CCA1 over-expressing seedlings rescues root growth. Thus, a circadian rheostat orchestrates electrochemical signals to optimize source capacity with sink demand.
2025-12-30 | GSE315134 | GEO
Project description:The phytohormone auxin controls a myriad of processes in plants, at least in part through its regulation of cell expansion. The "acid growth hypothesis" has been proposed to explain auxin-stimulated cell expansion for five decades, but the mechanism underlying auxin-induced cell wall acidification is poorly characterized. Auxin induces the phosphorylation and activation of the plasma membrane (PM) H+-ATPase that pumps protons into the apoplast, yet how auxin activates its phosphorylation remains elusive. Here, we show that the transmembrane kinase (TMK) auxin signaling proteins interact with PM H+-ATPases and activate their phosphorylation to promote cell wall acidification and hypocotyl cell elongation in Arabidopsis. Auxin induced TMK's interaction with H+-ATPase on the plasma membrane within 1-2 minutes as well as TMK-dependent phosphorylation of the penultimate Thr residue. Genetic, biochemical, and molecular evidence demonstrates that TMKs directly phosphorylate PM H+-ATPase and are required for auxin-induced PM H+-ATPase activation, apoplastic acidification, and cell expansion. Thus, our findings reveal a crucial connection between auxin and PM H+-ATPase activation in regulating apoplastic pH changes and cell expansion via TMK-based cell surface auxin signaling.
2021-07-14 | MSV000087822 | MassIVE
Project description:The size and shape of plant organs are highly responsive to environmental conditions. The plant's embryonic stem, or hypocotyl, displays phenotypic plasticity, in response to light and temperature. The, hypocotyl of shade avoiding species elongate to outcompete neighbouring plants and secure access to sunlight. Similar elongation occurs in high temperature. PHYTOCHROME-INTERACTING FACTORS (PIFs) family transcription are known to be importenet players in these responses. However, it is poorly understood how environmental light and temperature interact to affect plants development. We found that low R/FR combined with warm temperature produces a synergistic hypocotyl growth response that dependent on PIF7 and the hormone auxin. We demonstrate that additional, unknown factor/s must be working downstream of the phyB-PIF-auxin module. As shade responses are known to affect yield, susceptibility to pathogens, and fruit quality in many species, our findings will improve the predictions of how plants will respond to increased ambient temperatures when grown at high density, a condition in which mutual shading occurs.
2022-07-26 | GSE205208 | GEO
Project description:Growth of a complex multicellular organism requires coordinated changes in diverse cell types. These cellular changes generate organs of the correct size, shape and functionality. During plant development, the growth hormone auxin induces stem elongation; however, which cell types of the stem perceive the auxin signal and contribute to organ growth is poorly understood. Here, we show that auxin signalling is required in many cell types for correct hypocotyl stem growth, with a key role for the epidermis. Combining genetic manipulations in Arabidopsis thaliana with transcriptional profiling of the hypocotyl epidermis from Brassica rapa, we show that auxin functions in the epidermis in part by inducing activity of the locally-acting, growth-promoting brassinosteroid pathway. Our findings clarify cell-specific auxin function in the hypocotyl, and highlight the complexity of cell-type interactions within a growing organ. We performed whole-genome transcriptome (mRNA-Seq) on 5 d-old W light-grown Arabidopsis thaliana plants (CER6pro>>axr3-1::mCit experimental plants and UAS::axr3-1::mCit hemizygous control plants; whole-seedling tissue) treated for 4 h W light or low R:FR shade. In addition, we performed mRNA-Seq on 4 d-old Brassica rapa plants (FPsc strain) treated for 9 h W light or shade. Brassica tissues collected were hypocotyl epidermal peels or whole hypocotyls.
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Project description:MicroRNAs (miRNAs) play diverse roles in plant development, but whether and how miRNAs participate in thermomorphogenesis remains ambiguous. Here we show that HYPONASTIC LEAVES1 (HYL1) – a key component of microRNA biogenesis – acts downstream of the thermal regulator PHYTOCHROME INTERACTING FACTOR 4 in temperature-dependent plasticity of hypocotyl growth in Arabidopsis. A hyl1-2 suppressor screen identified a dominant dicer-like1 (dcl1) allele, dcl1-24, which rescues hyl1-2’s defects in miRNA biosynthesis and warm temperature-induced hypocotyl elongation. Genome-wide miRNA and transcriptome analysis reveal microRNA156 (miR156) and its target SQUAMOSA PROMOTER-BINDING-LIKE 9 (SPL9) as critical regulators of thermomorphogenesis. Surprisingly, perturbation of the miR156/SPL9 module disengages seedling responsiveness to warm temperatures by impeding auxin sensitivity. Moreover, the miR156-dependent auxin sensitivity also operates in the shade avoidance response at lower temperatures. Thus, these results unveil the miRNA156/SPL9 module as a previously-uncharacterized genetic circuitry that enables plant growth plasticity in response to environmental temperature and light changes.
2023-02-11 | GSE216361 | GEO
Project description:Driven by cell elongation, hypocotyl growth is tightly controlled by light and responds to both external stimuli and endogenous hormonal pathways. Hypocotyls are responsive to the stress signalling hormone abscisic acid (ABA), which effectively inhibits cell elongation. However, how this regulation is connected to light signalling has been a subject of limited studies. Here, we show that, contrary to light-grown seedlings, hypocotyl elongation of dark-grown seedlings is ABA-insensitive. In the dark, hypocotyl sensitivity to ABA is restored in the constitutive photomorphogenic pifq and cop1-4 mutants, suggesting that an active light signalling pathway is necessary for hypocotyl responsiveness to ABA. Surprisingly, etiolated hypocotyls retain an intact ABA signalling pathway, as could be detected by the induction of ABI1 and RD29B transcripts in response to exogenous ABA, suggesting that inhibition of hypocotyl elongation occurs through a divergent path that can be inhibited by PIFs. Here, using RNA-seq analysis we identified a number of ABA differentially expressed genes (DEGs) that correlate with ABA inhibition of hypocotyl elongation. Among these DEGs a number of SMALL AUXIN-UP RNA (SAUR) genes that are known to directly repress D-CLADE TYPE 2C PROTEIN PHOSPHATASES (PP2C.D) were found. The abrogation of PP2CD.D2-SAUR interaction in the pp2c.d2/PP2C.D2M331K -GFP line, restored ABA sensitivity in the dark, suggesting that SAUR proteins, upregulated by PIFs, are sufficient to render hypocotyls insensitive to ABA. This hypocotyl-specific mechanism enables to promote growth towards the light at all costs, overriding ABA inhibition of cell elongation, to ensure subsequent seedling establishment and survival.
2025-05-22 | GSE283262 | GEO
Project description:We hypothesized a convergence of transcriptome profiles in hypocotyls of low blue light (LB) or low red/far red light (LRFR) treated seedlings as both conditions trigger hypocotyl cell elongation. To test this hypothesis, we did a transcriptome analysis in of 5d-old long-day (LD)-grown Col-0 (wild type, WT), pif457, and yuc2589 seedlings treated for 3 hours with LB, LRFR or remaining in the same light condition (WL). We used dissected cotyledons and hypocotyls to characterize the LB and LRFR response in both organs and determine their dependency on PIFs and YUC-mediated auxin biosynthesis.
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Project description:MicroRNAs (miRNAs) play diverse roles in plant development, but whether and how miRNAs participate in thermomorphogenesis remains ambiguous. Here we show that HYPONASTIC LEAVES1 (HYL1) – a key component of microRNA biogenesis – acts downstream of the thermal regulator PHYTOCHROME INTERACTING FACTOR 4 in temperature-dependent plasticity of hypocotyl growth in Arabidopsis. A hyl1-2 suppressor screen identified a dominant dicer-like1 (dcl1) allele, dcl1-24, that rescues hyl1-2’s defects in miRNA biosynthesis and warm temperature-induced hypocotyl elongation. Genome-wide miRNA and transcriptome analysis reveal microRNA156 (miR156) and its target SQUAMOSA PROMOTER-BINDING-LIKE 9 (SPL9) as critical regulators of thermomorphogenesis. Surprisingly, perturbation of the miR156/SPL9 module disengages seedling responsiveness to warm temperatures by impeding auxin sensitivity. Moreover, the miR156-dependent auxin sensitivity also operates in the shade avoidance response at lower temperatures. Thus, these results unveil the miRNA156/SPL9 module as a previously-uncharacterized genetic circuitry that enables plant growth plasticity in response to environmental temperature and light changes.
2023-02-11 | GSE216360 | GEO
Project description:During de-etiolation of Arabidopsis seedlings, light promotes the expansion of cotyledons but inhibits the elongation of hypocotyls. The mechanism of this differential regulation of cell enlargement is unclear. Our organ-specific transcriptomic analysis identified 32 Small Auxin Up RNA (SAUR) genes whose transcripts were light-induced in cotyledons and/or repressed in hypocotyls. We therefore named these SAURs as lirSAURs. Both overexpression and mutation analyses demonstrated that lirSAURs could promote cotyledon expansion and opening and enhance hypocotyl elongation, possibly by inhibiting phosphatase activity of PP2C-Ds. Light reduced auxin levels to down-regulate the expression of lirSAURs in hypocotyls. Further, phytochrome-interacting factors (PIFs) were shown
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