Roles of auxin and ethylene in aerenchyma formation in sugarcane roots.

Although the cross-talk between auxin and ethylene has been described during plant development, the role played by auxin upon gene expression during aerenchyma formation is poorly understood. Root aerenchyma formation results from the opening of gas spaces in the cortex. It is part of a developmental program (constitutive) or due to ethylene treatment or abiotic stress (induced) such as flooding and nutrient starvation. This process relies on programmed cell death and cell wall modifications. Here we followed development of aerenchyma formation in sugarcane along 5 cm from the root apex. As a constitutive process, the aerenchyma formation was observed in the cortex from the 3rd cm onwards. This occurred despite 1-methylcyclepropene (1-MCP) treatment, an inhibitor of ethylene perception. However, this process occurred while ethylene (and auxin) levels decreased. Within the aerenchyma formation zone, the concentration of ethylene is lower in comparison to the concentration in maize. Besides, the ratio between both hormones (ethylene and auxin) was around 1:1. These pieces of evidence suggest that ethylene sensitivity and ethylene-auxin balance may play a role in the formation of aerenchyma. Furthermore, the transcriptional analysis showed that genes related to cell expansion are up-regulated due to 1-MCP treatment. Our results help explaining the regulation of the formation constitutive aerenchyma in sugarcane.

Efficacy of geraniol but not of β-ionone or their combination for the chemoprevention of rat colon carcinogenesis

β-ionone (βI), a cyclic isoprenoid, and geraniol (GO), an acyclic monoterpene, represent a promising class of dietary chemopreventive agents against cancer, whose combination could result in synergistic anticarcinogenic effects. The chemopreventive activities of βI and GO were evaluated individually or in combination during colon carcinogenesis induced by dimethylhydrazine in 48 3-week-old male Wistar rats (12 per group) weighing 40-50 g. Animals were treated for 9 consecutive weeks with βI (16 mg/100 g body weight), GO (25 mg/100 g body weight), βI combined with GO or corn oil (control). Number of total aberrant crypt foci (ACF) and of ACF ≥4 crypts in the distal colon was significantly lower in the GO group (66 ± 13 and 9 ± 2, respectively) compared to control (102 ± 9 and 17 ± 3) and without differences in the βI (91 ± 11 and 14 ± 3) and βI+GO groups (96 ± 5 and 19 ± 2). Apoptosis level, identified by classical apoptosis morphological criteria, in the distal colon was significantly higher in the GO group (1.64 ± 0.06 apoptotic cells/mm²) compared to control (0.91 ± 0.07 apoptotic cells/mm²). The GO group presented a 0.7-fold reduction in Bcl-2 protein expression (Western blot) compared to control. Colonic mucosa concentrations of βI and GO (gas chromatography/mass spectrometry) were higher in the βI and GO groups, respectively, compared to the control and βI+GO groups. Therefore, GO, but not βI, represents a potential chemopreventive agent in colon carcrvpdate=20110329inogenesis. Surprisingly, the combination of isoprenoids does not represent an efficient chemopreventive strategy.

Efficacy of geraniol but not of ß-ionone or their combination for the chemoprevention of rat colon carcinogenesis.

ß-ionone (ßI), a cyclic isoprenoid, and geraniol (GO), an acyclic monoterpene, represent a promising class of dietary chemopreventive agents against cancer, whose combination could result in synergistic anticarcinogenic effects. The chemopreventive activities of ßI and GO were evaluated individually or in combination during colon carcinogenesis induced by dimethylhydrazine in 48 3-week-old male Wistar rats (12 per group) weighing 40-50 g. Animals were treated for 9 consecutive weeks with ßI (16 mg/100 g body weight), GO (25 mg/100 g body weight), ßI combined with GO or corn oil (control). Number of total aberrant crypt foci (ACF) and of ACF ≥4 crypts in the distal colon was significantly lower in the GO group (66 ± 13 and 9 ± 2, respectively) compared to control (102 ± 9 and 17 ± 3) and without differences in the ßI (91 ± 11 and 14 ± 3) and ßI+GO groups (96 ± 5 and 19 ± 2). Apoptosis level, identified by classical apoptosis morphological criteria, in the distal colon was significantly higher in the GO group (1.64 ± 0.06 apoptotic cells/mm²) compared to control (0.91 ± 0.07 apoptotic cells/mm²). The GO group presented a 0.7-fold reduction in Bcl-2 protein expression (Western blot) compared to control. Colonic mucosa concentrations of ßI and GO (gas chromatography/mass spectrometry) were higher in the ßI and GO groups, respectively, compared to the control and ßI+GO groups. Therefore, GO, but not ßI, represents a potential chemopreventive agent in colon carcinogenesis. Surprisingly, the combination of isoprenoids does not represent an efficient chemopreventive strategy.

Inhibition of beta-amylase activity, starch degradation and sucrose formation by indole-3-acetic acid during banana ripening.

In order to observe the effect of indole-3-acetic acid (IAA) on carbohydrate metabolism, unripe banana (Musa acuminata AAA, cv. Nanicão) slices were infiltrated with the hormone and left to ripen under controlled conditions. The climacteric respiration burst was reduced by the action of IAA, and starch degradation and sucrose formation were delayed. Sucrose synthase (SuSy; EC 2.4.1.13) and sucrose-phosphate synthase (SPS; EC 2.4.1.14) activities and transcript levels were not affected, indicating that prevention of sucrose accumulation was not related to sucrose-metabolizing enzymes. Impairment of sucrose synthesis could be a consequence of lack of substrate, since starch degradation was inhibited. The increase in activity and transcript level of beta-amylase was delayed, indicating that this enzyme could be important in starch-to-sucrose metabolism in bananas and that it might be, at least partially, controlled at the transcriptional level. This is the first report showing that IAA can delay starch degradation, possibly affecting the activity of hydrolytic enzymes such as beta-amylase (EC 3.2.1.2).