Hydrogen cyanide is a volatile modulator of bacterial behaviour
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB53421 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR9830980.fastq.gz | Fastqsanger.gz | |||
| ERR9832950.fastq.gz | Fastqsanger.gz | |||
| ERR9830981.fastq.gz | Fastqsanger.gz | |||
| ERR9832441.fastq.gz | Fastqsanger.gz | |||
| ERR9832881.fastq.gz | Fastqsanger.gz |
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Project description:hydrogen-producing bacterial consortium overview
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Project description:Perennial plants, like fruit trees grown in temperate regions, are characterized by bud dormancy, a rest state that protects the bud from cold during winter. At the same time, these plants have developed a requirement for winter chill for correct flowering. However, winters are becoming increasingly warm in temperate regions, resulting in dramatic effects on the flowering output and therefore crop yield. A compound that successfully compensates for missing winter chill is hydrogen cyanamide, which has been used to synchronize and advance flowering time in a range of commercially important fruit crops. Hydrogen cyanamide also represents a unique tool for researchers to study controlled endodormancy release. Here, we treated dormant sweet cherry flower buds with hydrogen cyanamide, sampling flower buds at different time points after treatment. RNAseq revealed more than 6,000 hydrogen cyanamide-responsive genes. In accordance with these results, hydrogen cyanamide treatment increased the levels of jasmonoyl-isoleucine (JA-Ile) and the cytokinins trans-zeatin riboside (tZR), dihydrozeatin (DZ) and dihydrozeatin riboside (DZR). Furthermore, hydrogen cyanamide affected the expression of antioxidant- and cell wall loosening-associated transcripts. These results suggest a complex mechanism of action for hydrogen cyanamide-induced endodormancy release, including key roles for JA-Ile, zeatin-type cytokinins and hydrogen cyanide.
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Project description:Plants perceive herbivory induced volatiles and respond to them by upregulating their defenses. So far, the organs responsible for volatile perception remain poorly described. Here, we show that responsiveness to the herbivory induced green leaf volatile (Z)-3-hexenyl acetate (HAC) in terms of volatile emission, transcriptional regulation and jasmonate defense hormone activation is largely constrained to younger maize leaves. Older leaves are much less sensitive to HAC. In a given leaf, responsiveness to HAC is high at immature developmental stages and drops off rapidly during maturation. Responsiveness to the non-volatile elicitor ZmPep3 shows an opposite pattern, demonstrating that this form of hyposmia (i.e. decreased sense of smell) is not due to a general defect in jasmonate defense signaling in mature leaves. Neither stomatal conductance nor leaf cuticle composition explain the unresponsiveness of older leaves to HAC, suggesting perception mechanisms upstream of jasmonate signaling as driving factors. Finally, we show that hyposmia in older leaves is not restricted to HAC, and extends to the full blend of herbivory induced volatiles. In conclusion, our work identifies immature maize leaves as dominant stress volatile sensing organs. The tight spatiotemporal control of volatile perception may facilitate within-plant defense signaling to protect young leaves, and may allow plants with complex architectures to explore the dynamic odor landscapes at the outer periphery of their shoots
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