3,524 research outputs found

    Functional characterization of TRICHOMELESS2, a new single-repeat R3 MYB transcription factor in the regulation of trichome patterning in Arabidopsis

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    <p>Abstract</p> <p>Background</p> <p>Single-repeat R3 MYB transcription factors (single-repeat MYBs) play important roles in controlling trichome patterning in <it>Arabidopsis</it>. It was proposed that single-repeat MYBs negatively regulate trichome formation by competing with GLABRA1 (GL1) for binding GLABRA3/ENHANCER OF GLABRA3 (GL3/EGL3), thus inhibiting the formation of activator complex TTG1(TRANSPARENT TESTA GLABRA1)-GL3/EGL3-GL1 that is required for the activation of <it>GLABRA2 </it>(<it>GL2</it>), whose product is a positive regulator of trichome formation. Previously we identified a novel single-repeat MYB transcription factor, TRICHOMELESS1 (TCL1), which negatively regulates trichome formation on the inflorescence stems and pedicels by directly suppressing the expression of <it>GL1</it>.</p> <p>Results</p> <p>We analyzed here the role of TRICHOMELESS2 (TCL2), a previously-uncharacterized single-repeat MYB transcription factor in trichome patterning in <it>Arabidopsis</it>. We showed that TCL2 is closely related to TCL1, and like TCL1 and other single-repeat MYBs, TCL2 interacts with GL3. Overexpression of <it>TCL2 </it>conferred glabrous phenotype while knockdown of <it>TCL2 </it>via RNAi induced ectopic trichome formation on the inflorescence stems and pedicels, a phenotype that was previously observed in <it>tcl1 </it>mutants. These results suggested that TCL2 may have overlapping function with TCL1 in controlling trichome formation on inflorescences. On the other hand, although the transcription of <it>TCL2</it>, like <it>TCL1, </it>is not controlled by the activator complex formed by GL1 and GL3, and TCL2 and TCL1 proteins are more than 80% identical at the amino acid level, the expression of <it>TCL2 </it>under the control of <it>TCL1 </it>promoter only partially recovered the mutant phenotype of <it>tcl1</it>, implying that TCL2 and TCL1 are not fully functional equivalent.</p> <p>Conclusions</p> <p>TCL2 function redundantly with TCL1 in controlling trichome formation on inflorescences, but they are not fully functional equivalent. Transcription of <it>TCL2 </it>is not controlled by activator complex formed by GL1 and GL3, but <it>MIR156 </it>controlled SQUAMOSA PROMOTER BINDING PROTEIN LIKE (SPL) transcription factors. However, SPLs might require co-activators to regulate the expression of their target genes, including <it>TCL1</it>, <it>TRY </it>and possibly, <it>TCL2</it>.</p

    Antagonistic actions of boron against inhibitory effects of aluminum toxicity on growth, CO2 assimilation, ribulose-1,5-bisphosphate carboxylase/oxygenase, and photosynthetic electron transport probed by the JIP-test, of Citrus grandis seedlings

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    <p>Abstract</p> <p>Background</p> <p>Little information is available on the amelioration of boron (B) on aluminum (Al)-induced photosynthesis inhibition. Sour pummelo (<it>Citrus grandis</it>) seedlings were irrigated for 18 weeks with nutrient solution containing 4 B levels (2.5, 10, 25 and 50 μM H<sub>3</sub>BO<sub>3</sub>) × 2 Al levels (0 and 1.2 mM AlCl<sub>3</sub>·6H<sub>2</sub>O). The objectives of this study were to determine how B alleviates Al-induced growth inhibition and to test the hypothesis that Al-induced photosynthesis inhibition can be alleviated by B <it>via </it>preventing Al from getting into shoots.</p> <p>Results</p> <p>B had little effect on plant growth, root, stem and leaf Al, leaf chlorophyll (Chl), CO<sub>2 </sub>assimilation, ribulose-1,5-bisphosphate carboxylase/oxygenase (Rubisco), Chl a fluorescence (OJIP) transient and related parameters without Al stress except that root, stem and leaf B increased with increasing B supply and that 50 μM B decreased slightly root dry weight. Al-treated roots, stems and leaves displayed a higher or similar B. B did not affect root Al under Al stress, but decreased stem and leaf Al level. Shoot growth is more sensitive to Al stress than root growth, CO<sub>2 </sub>assimilation, Chl, Rubisco, OJIP transient and most related parameters. Al-treated leaves showed decreased CO<sub>2 </sub>assimilation, but increased or similar intercellular CO<sub>2 </sub>concentration. Both initial and total Rubisco activity in Al-treated leaves decreased to a lesser extent than CO<sub>2 </sub>assimilation. Al decreased maximum quantum yield of primary photochemistry and total performance index, but increased minimum fluorescence, K-band, relative variable fluorescence at J- and I-steps. B could alleviate Al-induced increase or decrease for all these parameters. Generally speaking, the order of B effectiveness was 25 μM > 10 μM ≥ 50 μM (excess B) > 2.5 μM.</p> <p>Conclusion</p> <p>We propose that Al-induced photosynthesis inhibition was mainly caused by impaired photosynthetic electron transport chain, which may be associated with growth inhibition. B-induced amelioration of root inhibition was probably caused by B-induced changes in Al speciation and/or sub-cellular compartmentation. However, B-induced amelioration of shoot and photosynthesis inhibition and photoinhibitory damage occurring at both donor and acceptor sides of photosystem II could be due to less Al accumulation in shoots.</p

    Hidden Tree Structure is a Key to the Emergence of Scaling in the World Wide Web

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    Preferential attachment is the most popular explanation for the emergence of scaling behavior in the World Wide Web, but this explanation has been challenged by the global information hypothesis, the existence of linear preference and the emergence of new big internet companies in the real world. We notice that most websites have an obvious feature that their pages are organized as a tree (namely hidden tree) and hence propose a new model that introduces a hidden tree structure into the Erd\H{o}s-R\'e}yi model by adding a new rule: when one node connects to another, it should also connect to all nodes in the path between these two nodes in the hidden tree. The experimental results show that the degree distribution of the generated graphs would obey power law distributions and have variable high clustering coefficients and variable small average lengths of shortest paths. The proposed model provides an alternative explanation to the emergence of scaling in the World Wide Web without the above-mentioned difficulties, and also explains the "preferential attachment" phenomenon.Comment: 4 Pages, 7 Figure

    Spectroscopy of q3qˉ3\rm{q}^3\bar{\rm{q}}^3-States in Quark Model and Baryon-Antibaryon Enhancements

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    We study the mass spectrum of the q3qˉ3\rm{q}^3\bar{\rm{q}}^3 mesons both from the quark model with triquark correlations and from common quark model with colormagnetic interactions and with relative S-waves between quarks. Two cluster configurations (q3)(qˉ3)(\rm{q}^3)-(\bar{\rm{q}}^3) and (q2qˉ)(qqˉ2)(\rm{q}^2\bar{\rm{q}})-(\rm{q}\bar{\rm{q}}^2) are considered. In the spectrum we find rather stable states which have the same quantum number with particle resonances which are corresponding to the ppˉp\bar{p} enhancement, pΛˉp\bar{\Lambda} enhancement and ΛΛˉ\Lambda\bar{\Lambda} enhancement with spin-0\mathbf{0} or 1\mathbf{1}. This imply these enhancements are NOT experimental artifacts. The color-spin-flavor structures of ppˉp\bar{p}, pΛˉp\bar{\Lambda}, and ΛΛˉ\Lambda\bar{\Lambda} enhancements are revealed. The existence of spin-1\mathbf{1} ΛΛˉ,pΛˉ,ppˉ\Lambda\bar{\Lambda}, p\bar{\Lambda}, p\bar{p} enhancements is predicted.Comment: 45 pages, 5 figure

    Arabidopsis Receptor of Activated C Kinase1 Phosphorylation by WITH NO LYSINE8 KINASE

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    Receptor of activated C kinase1 (RACK1) is a versatile scaffold protein that binds to numerous proteins to regulate diverse cellular pathways in mammals. In Arabidopsis (Arabidopsis thaliana), RACK1 has been shown to regulate plant hormone signaling, stress responses, and multiple processes of growth and development. However, little is known about the molecular mechanism underlying these regulations. Here, we show that an atypical serine (Ser)/threonine (Thr) protein kinase, WITH NO LYSINE8 (WNK8), phosphorylates RACK1. WNK8 physically interacted with and phosphorylated RACK1 proteins at two residues: Ser-122 and Thr-162. Genetic epistasis analysis of rack1 wnk8 double mutants indicated that RACK1 acts downstream of WNK8 in the glucose responsiveness and flowering pathways. The phosphorylation-dead form, RACK1AS122A/T162A, but not the phosphomimetic form, RACK1AS122D/T162E, rescued the rack1a null mutant, implying that phosphorylation at Ser-122 and Thr-162 negatively regulates RACK1A function. The transcript of RACK1AS122D/T162E accumulated at similar levels as those of RACK1S122A/T162A. However, although the steady-state level of the RACK1AS122A/T162A protein was similar to wild-type RACK1A protein, the RACK1AS122D/T162E protein was nearly undetectable, suggesting that phosphorylation affects the stability of RACK1A proteins. Taken together, these results suggest that RACK1 is phosphorylated by WNK8 and that phosphorylation negatively regulates RACK1 function by influencing its protein stability

    A role of corazonin receptor in larval-pupal transition and pupariation in the oriental fruit fly Bactrocera dorsalis (Hendel) (Diptera: Tephritidae)

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    Corazonin (Crz) is a neuropeptide hormone, but also a neuropeptide modulator that is internally released within the CNS, and it has a widespread distribution in insects with diverse physiological functions. Here, we identified and cloned the cDNAs of Bactrocera dorsalis that encode Crz and its receptor CrzR. Mature BdCrz has 11 residues with a unique Ser11 substitution (instead of the typical Asn) and a His in the evolutionary variable position 7. The BdCrzR cDNA encodes a putative protein of 608 amino acids with 7 putative transmembrane domains, typical for the structure of G-protein-coupled receptors. When expressed in Chinese hamster ovary (CHO) cells, the BdCrzR exhibited a high sensitivity and selectivity for Crz (EC50 approximate to 52.5 nM). With qPCR, the developmental stage and tissue-specific expression profiles in B. dorsalis demonstrated that both BdCrz and BdCrzR were highly expressed in the larval stage, and BdCrzR peaked in 2-day-old 3rd-instar larvae, suggesting that the BdCrzR may play an important role in the larval-pupal transition behavior. Immunochemical localization confirmed the production of Crz in the central nervous system (CNS), specifically by a group of three neurons in the dorso-lateral protocerebrum and eight pairs of lateral neurons in the ventral nerve cord. qPCR analysis located the BdCrzR in both the CNS and epitracheal gland, containing the Inka cells. Importantly, dsRNA-BdCrzR-mediated gene-silencing caused a delay in larval-pupal transition and pupariation, and this phenomenon agreed with a delayed expression of tyrosine hydroxylase and dopa-decarboxylase genes. We speculate that CrzR-silencing blocked dopamine synthesis, resulting in the inhibition of pupariation and cuticular melanization. Finally, injection of Crz in head-ligated larvae could rescue the effects. These findings provide a new insight into the roles of Crz signaling pathway components in B. dorsalis and support an important role of CrzR in larval-pupal transition and pupariation behavior
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