Shoot circumnutation and winding movements require gravisensing cells. (1/13)

Circumnutation and winding in plants are universal growth movements that allow plants to survive despite their sessile nature. However, the detailed molecular mechanisms controlling these phenomena remain unclear. We previously found that a gravitropic mutant of Japanese morning glory (Pharbitis nil or Ipomoea nil), Shidare-asagao (weeping), is defective not only in circumnutation but also in the winding response. This phenotype is similar to that of the Arabidopsis SCARECROW (SCR) mutant. We therefore investigated whether morning glory SCR (PnSCR) is involved in the weeping phenotype. We found that one amino acid was inserted into the highly conserved VHIID motif in weeping-type PnSCR; this mutation caused abnormal endodermal differentiation. We introduced either the mutant or WT PnSCR into Arabidopsis scr mutants for complementation tests. PnSCR of the WT, but not of weeping, rescued the shoot gravitropism and circumnutation of scr. These results show that both the abnormal gravitropism and the circumnutation defect in weeping are attributable to a loss of PnSCR function. Thus, our data show that gravisensing endodermal cells are indispensable for shoot circumnutation and the winding response and that PnSCR is responsible for the abnormal phenotypes of weeping.  (+info)

A reappraisal of the role of abscisic acid and its interaction with auxin in apical dominance. (2/13)

BACKGROUND AND AIMS: Evidence from pea rms1, Arabidopsis max4 and petunia dad1 mutant studies suggest an unidentified carotenoid-derived/plastid-produced branching inhibitor which moves acropetally from the roots to the shoots and interacts with auxin in the control of apical dominance. Since the plant hormone, abscisic acid (ABA), known to inhibit some growth processes, is also carotenoid derived/plastid produced, and because there has been indirect evidence for its involvement with branching, a re-examination of the role of ABA in apical dominance is timely. Even though it has been determined that ABA probably is not the second messenger for auxin in apical dominance and is not the above-mentioned unidentified branching inhibitor, the similarity of their derivation suggests possible relationships and/or interactions. METHODS: The classic Thimann-Skoog auxin replacement test for apical dominance with auxin [0.5 % naphthalene acetic acid (NAA)] applied both apically and basally was combined in similar treatments with 1 % ABA in Ipomoea nil (Japanese Morning Glory), Solanum lycopersicum (Better Boy tomato) and Helianthus annuus (Mammoth Grey-striped Sunflower). KEY RESULTS: Auxin, apically applied to the cut stem surface of decapitated shoots, strongly restored apical dominance in all three species, whereas the similar treatment with ABA did not. However, when ABA was applied basally, i.e. below the lateral bud of interest, there was a significant moderate repression of its outgrowth in Ipomoea and Solanum. There was also some additive repression when apical auxin and basal ABA treatments were combined in Ipomoea. CONCLUSION: The finding that basally applied ABA is able partially to restore apical dominance via acropetal transport up the shoot suggests possible interactions between ABA, auxin and the unidentified carotenoid-derived branching inhibitor that justify further investigation.  (+info)

Triterpenoid saponins from the seeds of Pharbitis nil. (3/13)

From the seeds of Pharbitis nil (Convolvulaceae), two new oleanene-type triterpene glycosides, pharbitosides A (1) and B (2), together with beta-sitosterol, beta-sitosterol glucoside (daucosterol), caffeic acid, and methyl caffeate were isolated. The structure of pharbitoside A (1) was elucidated to be queretaroic acid 3-O-alpha-L-rhamnopyranosyl-(1-->2)-O-beta-D-glucopyranosyl-(1-->2)-beta-D-glucop yranoside (1). Pharbitoside B (2) is a 21alpha-hydroxyoleanolic acid saponin carrying the same sugar moiety as that of pharbitoside A (1).  (+info)

InPSR26, a putative membrane protein, regulates programmed cell death during petal senescence in Japanese morning glory. (4/13)


Autophagy regulates progression of programmed cell death during petal senescence in Japanese morning glory. (5/13)

Petal senescence is a type of programmed cell death (PCD) that is tightly regulated by multiple genes. We recently reported that a putative membrane protein, InPSR26, regulates progression of PCD during petal senescence in Japanese morning glory (Ipomoea nil). Reduced InPSR26 expression in transgenic plants (PSR26r lines) resulted in accelerated petal senescence with hastened development of PCD symptoms, and transcript levels of autophagy-related genes were reduced in the petals. Autophagy visualized by monodansylcadaverine staining indicated reduced autophagic activity in the PSR26r plants. The results from our recent studies suggest that InPSR26 acts to delay the progression of PCD during petal senescence, possibly through regulation of the autophagic process. In this addendum, we discuss the role of autophagy in petal senescence as it relates to these findings.  (+info)

Expression of allene oxide cyclase from Pharbitis nil upon theobroxide treatment. (6/13)

In previous reports we have reported that theobroxide induces characteristic accumulation of allene oxide cyclase (AOC; EC protein and jasmonic acid (JA) in Pharbitis nil. In the present study, PnAOC, an AOC gene from Pharbitis nil was cloned. Immunofluorescence assays indicated that the AOC protein is located in the chloroplast of vascular bundles in Pharbitis nil leaves. The PnAOC cDNA sequence lacking the chloroplast signal peptide was successfully expressed in Escherichia coli, and a gas chromatography-mass spectrum assay suggested the relative AOC activity of the recombinant PnAOC protein in comparison with Arabidopsis AOC2. Interestingly, a biphasic expression of PnAOC was induced by theobroxide, which is consistent with the accumulation patterns of AOC protein and JA. All these results indicate that AOC is the primary target of theobroxide regulation and suggest that feedback regulation of PnAOC by JA occurs upon theobroxide treatment in Pharbitis nil.  (+info)

Carotenoid composition and carotenogenic gene expression during Ipomoea petal development. (7/13)


Epigenetic regulation of photoperiodic flowering. (8/13)

The cytidine analogue 5-azacytidine, which causes DNA demethylation, induced flowering in the non-vernalization-requiring plants Perilla frutescens var. crispa, Silene armeria and Pharbitis nil (synonym Ipomoea nil) under non-inductive photoperiodic conditions, suggesting that the expression of photoperiodic flowering-related genes is regulated epigenetically by DNA methylation. The flowering state induced by DNA demethylation was not heritable. Changes in the genome-wide methylation state were examined by methylation-sensitive amplified fragment length polymorphism analysis. This analysis indicated that the DNA methylation state was altered by the photoperiodic condition. DNA demethylation also induced dwarfism, and the induced dwarfism of P. frutescens was heritable.  (+info)