Project description:Onion is regarded as non-climacteric. In onion, ethylene can suppress sprouting however, the ethylene binding inhibitor, 1-MCP can also suppress sprout growth although it is unknown how ethylene and 1-MCP elicit the same response. In this study, onion bulbs were treated with 10 μL L-1 ethylene or 1 μL L-1 1-MCP individually or in combination for 24 h at 20°C before or after curing (six weeks) at 20 or 28°C then stored at 1°C. Following curing, a subset of these same onion bulbs was stored separately under continuous air or ethylene (10 μL L-1) at 1°C
Project description:Onion is regarded as non-climacteric. In onion, ethylene can suppress sprouting however, the ethylene binding inhibitor, 1-MCP can also suppress sprout growth although it is unknown how ethylene and 1-MCP elicit the same response. In this study, onion bulbs were treated with 10 μL L-1 ethylene or 1 μL L-1 1-MCP individually or in combination for 24 h at 20°C before or after curing (six weeks) at 20 or 28°C then stored at 1°C. Following curing, a subset of these same onion bulbs was stored separately under continuous air or ethylene (10 μL L-1) at 1°C Six treatments were chosen for microarray analysis; four samples were taken before curing immediately after treatment with ethylene or 1-MCP or ethylene and 1-MCP in combination for 24 h at 20°C. The other two samples and two were taken at the end of storage following 6 weeks curing at 28°C andafter 29 weeks cold storage (1°C) in continuous air or continuous ethylene totalling 35 weeks storage. The four pre-curing samples used were untreated (control) or treated with EB, MB or EMB and the two samples after storage were control bulbs stored in continuous ethylene or air at 1°C. There were three biological replicates of each of the six treatments making 18 samples in total.
Project description:The type 1 taste receptor member 3 (T1R3) is a G protein-coupled receptor involved in sweet-taste perception. Besides the tongue, the T1R3 receptor is highly expressed in brain areas implicated in cognition, including the hippocampus and cortex. As cognitive decline is often preceded by significant metabolic or endocrinological dysfunctions regulated by the sweet-taste perception system, we hypothesized that a disruption of the sweet-taste perception in the brain could have a key role in the development of cognitive dysfunction. To assess the importance of the sweet-taste receptors in the brain, we conducted transcriptomic and proteomic analyses of cortical and hippocampal tissues isolated from T1R3 knock-out (T1R3KO) mice. The effect of an impaired sweet-taste perception system on cognition functions were examined by analyzing synaptic integrity and performing animal behavior on T1R3KO mice. Although T1R3KO mice did not present a metabolically disrupted phenotype, bioinformatic interpretation of the high-dimensionality data indicated a strong neurodegenerative signature associated with significant alterations in pathways involved in neuritogenesis, dendritic growth, and synaptogenesis. Furthermore, a significantly reduced dendritic spine density was observed in T1R3KO mice together with alterations in learning and memory functions as well as sociability deficits. Taken together our data suggest that the sweet-taste receptor system plays an important neurotrophic role in the extralingual central nervous tissue that underpins synaptic function, memory acquisition, and social behavior.