Auxin regulates lateral meristem activation in developing gametophytes of Ceratopteris richardii

This study investigates the auxin regulation of lateral meristem activation in the gametophytes of the fern Ceratopteris richardii Brongn. Exogenous auxin in the form of α-naphthaleneacetic acid or 2,4,5-trichlorophenoxy-acetic acid repressed the activation of the lateral meristem, and generated a male-like body plan. The auxin antagonist p-chlorophenoxyisobutyric acid reduced activity of both the apical and lateral meristems, and produced a circular-shaped gametophyte. Disrupting auxin transport with 2,3,5-triiodobenzoic acid led to a time lag in lateral meristem activation, while disrupting auxin transport with n-1-naphthylphthalamic acid produced several different body plans generated by the formation of a second lateral meristem. These findings suggest auxin mediates the activation of the lateral meristem and regulates lateral meristem function. In addition, auxin transport may be necessary for communication between the lateral meristem and other regions of the developing gametophyte. Auxin also controls the position of rhizoids produced by the gametophyte, and exogenous auxin interferes with the sexual differentiation of the gametophyte. These results are summarized in a model of how auxin regulates lateral meristem activation and meristem activity during gametophyte development in C. richardii.

Auxin-induced developmental patterns in Brassica juncea embryos

To investigate the mechanism of auxin action during pattern formation in dicot embryos, we tested the effects of the natural auxin indole-3-acetic acid (IAA), the auxin transport inhibitor N-(1-naphthyl)thalamic acid (NPA) and the antiauxin p-chlorophenoxyisobutyric acid (PCIB). In vitro treatments of isolated zygotic Brassica juncea embryos with these substances led to a wide range of morphogenetic alterations. Treatment of globular embryos with exogenous auxin (10-40 microM) either completely inhibited morphogenesis, resulting in ball-shaped embryos, or caused the development of egg- and cucumber-shaped embryos, which only consisted of a shortened hypocotyl without any apical structures. Axis duplication was observed sometimes after inhibition of auxin transport in globular embryos, and led to the development of twin embryos. During the transition from globular to heart stage, changes in auxin distribution or activity frequently caused the development of either split-collar or collar-cotyledons. Antiauxin inhibited cotyledon growth, leading to embryos with single or no cotyledons, or inhibited the development of the hypocotyl and the radicle. Inhibition of auxin transport in transition embryos sometimes led to axis broadening, which resulted in the development of two radicles. The described changes in embryo shapes represent arrests in different auxin-regulated developmental steps and phenocopy some Arabidopsis morphogenetic mutants.

PCIB Enhances Regeneration of Ipomoea cordatotriloba Dennstedt Leaf Explants and Protoplasts

Leaf callus of Ipomoea cordatotriloba was initiated by culturing explants on Linsmaier and Skoog medium containing 3 g yeast extract/liter, 18.9 μm ABA, 2.3 μm 2,4-D, and 0.15 m sucrose. Calluses were transferred to Murashige and Skoog media containing 17.8 μm BA and 0, 1, 10, or 100 μm PCIB. The number of shoots from calluses grown on medium containing 10 μm PCIB increased significantly, and the percentage of calluses exhibiting shoot regeneration almost doubled compared to calluses grown on regeneration medium without PCIB. Protoplasts isolated from stem and petiole tissues of in vitro-grown plants were cultured in Kao and Michayluk 8p medium to the callus stage. Calluses (4-6 mm) were transferred to the callus induction and regeneration media used to regenerate leaf-explant callus. Of the protoplast-derived calluses cultured on media containing 10 or 100 μm PCIB, ≈13% and 18%, respectively, regenerated shoots after 2 months; none regenerated on the medium without PCIB. Chemical names used: abscisic acid (ABA); 2,4-dichlorophenoxyacetic acid (2,4-D); N6-benzyladenine (BA); α -p-chlorophenoxyisobutyric acid (PCIB).

Alterations by peroxisome proliferators of acyl composition of hepatic phosphatidylcholine in rats, mice and guinea-pigs. Role of stearoyl-CoA desaturase

Rats, mice and guinea-pigs were administered p-chlorophenoxyisobutyric acid (clofibric acid) or 2,2′-(decamethylenedithio)diethanol (tiadenol). The treatments of rats and mice with either clofibric acid or tiadenol increased markedly the activities of stearoyl-CoA desaturase, palmitoyl-CoA chain elongation, 1-acylglycerophosphate (1-acyl-GP) acyltransferase and 1-acylglycerophosphocholine (1-acyl-GPC) acyltransferase, but not 2-acylglycerophosphocholine (2-acyl-GPC) acyltransferase in liver microsomes. The treatment of guinea-pigs with clofibric acid did not cause any change in the activities of these enzymes. The treatment of guinea-pigs with tiadenol caused a slight, but significant, increase in the activities of 1-acyl-GP acyltransferase and 1-acyl-GPC acyltransferase. The treatment of rats and mice with either clofibric acid or tiadenol increased markedly the proportion of 18:1 and decreased greatly the proportion of 18:0 in liver microsomal phosphatidylcholine. However, there is a considerable difference in the effects of the two peroxisome proliferators on the composition of polyunsaturated fatty acids in phosphatidylcholine between rats and mice. The treatment of guinea-pigs with either of the two peroxisome proliferators caused no change in acyl composition of phosphatidylcholine. The possible role of stearoyl-CoA desaturation in the regulation of acyl composition of phosphatidylcholine was discussed.