Publications - Cell and Metabolic Biology

Plants have the ability to alleviate the harmful effects caused by abiotic and biotic stress. Phytohormones play a very important role in the acclimation to these stresses. To study the role of jasmonate in the acclimation to osmotic stress, an ALLENE OXIDE CYCLASE (AOC) mutant of rice (cpm2), disrupted in the biosynthesis of jasmonic acid (JA), and its wild type (WT) background were employed to investigate their responses to osmotic stress caused by treatment with polyethylene glycol (PEG) 6000. WT showed tolerance to osmotic stress, correlated with a fast transient increase of JA and JA-isoleucine (JA-Ile) in the shoots prior to an increase in abscisic acid (ABA), followed by a second increase in jasmonates when exposing to osmotic stress during 24 h. In roots, the pattern of hormonal increase was similar, but the response appeared to be faster, and remained transient, also with respect to low levels of jasmonates upon continuing osmotic stress. The mutant, which was containing extremely low levels of jasmonates, was hypersensitive to the stress. However, ABA accumulated in both, shoots and roots of cpm2, to similar (but not equal) levels as those seen in the WT, demonstrating that the biosynthesis or catabolism of ABA in response to osmotic stress is at least partially independent of JA, but can be modulated by JA. Our results suggest that jasmonates operate in parallel, presumably synergistically, to ABA, and are indispensable for osmotic stress tolerance in rice.

Soil pollutants may affect root growth through interactions among phytohormones like auxin and jasmonates. Rice is frequently grown in paddy fields contaminated by cadmium and arsenic, but the effects of these pollutants on jasmonates/auxin crosstalk during adventitious and lateral roots formation are widely unknown. Therefore, seedlings of Oryza sativa cv. Nihonmasari and of the jasmonate-biosynthetic mutant coleoptile photomorphogenesis2 were exposed to cadmium and/or arsenic, and/or jasmonic acid methyl ester, and then analysed through morphological, histochemical, biochemical and molecular approaches.In both genotypes, arsenic and cadmium accumulated in roots more than shoots. In the roots, arsenic levels were more than twice higher than cadmium levels, either when arsenic was applied alone, or combined with cadmium. Pollutants reduced lateral root density in the wild -type in every treatment condition, but jasmonic acid methyl ester increased it when combined with each pollutant. Interestingly, exposure to cadmium and/or arsenic did not change lateral root density in the mutant. The transcript levels of OsASA2 and OsYUCCA2, auxin biosynthetic genes, increased in the wild-type and mutant roots when pollutants and jasmonic acid methyl ester were applied alone. Auxin (indole-3-acetic acid) levels transiently increased in the roots with cadmium and/or arsenic in the wild-type more than in the mutant. Arsenic and cadmium, when applied alone, induced fluctuations in bioactive jasmonate contents in wild-type roots, but not in the mutant. Auxin distribution was evaluated in roots of OsDR5::GUS seedlings exposed or not to jasmonic acid methyl ester added or not with cadmium and/or arsenic. The DR5::GUS signal in lateral roots was reduced by arsenic, cadmium, and jasmonic acid methyl ester. Lipid peroxidation, evaluated as malondialdehyde levels, was higher in the mutant than in the wild-type, and increased particularly in As presence, in both genotypes.Altogether, the results show that an auxin/jasmonate interaction affects rice root system development in the presence of cadmium and/or arsenic, even if exogenous jasmonic acid methyl ester only slightly mitigates pollutants toxicity.

In the respirofermentative yeast Kluyveromyces lactis, only a single genetic locus encodes glucose transporters that can support fermentative growth. This locus is polymorphic in wild-type isolates carrying either KHT1and KHT2, two tandemly arranged HXT-like genes, or RAG1, a low-affinity transporter gene that arose by recombination between KHT1 andKHT2. Here we show that KHT1 is a glucose-induced gene encoding a low-affinity transporter very similar to Rag1p. Kht2p has a lower Km (3.7 mM) and a more complex regulation. Transcription is high in the absence of glucose, further induced by low glucose concentrations, and repressed at higher glucose concentrations. The response ofKHT1 and KHT2 gene regulation to high but not to low concentrations of glucose depends on glucose transport. The function of either Kht1p or Kht2p is sufficient to mediate the characteristic response to high glucose, which is impaired in akht1 kht2 deletion mutant. Thus, the KHTgenes are subject to mutual feedback regulation. Moreover, glucose repression of the endogenous β-galactosidase (LAC4) promoter and glucose induction of pyruvate decarboxylase were abolished in the kht1 kht2 mutant. These phenotypes could be partially restored by HXT gene family members fromSaccharomyces cerevisiae. The results indicate that the specific responses to high but not to low glucose concentrations require a high rate of glucose uptake.