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This is used to produce approximately 700 million kilograms yearly. Other syntheses that have been examined but not implemented include Wacker oxidation of 2-butene and oxidation of isobutylbenzene, which is analogous to the industrial production of acetone.[7] The cumene process can be modified to produce phenol and a mixture of acetone and butanone instead of only phenol and acetone in the original.[9]


As butanone dissolves polystyrene and many other plastics, it is sold as "model cement" for use in connecting parts of scale model kits. Though often considered an adhesive, it is actually functioning as a welding agent in this context.

Butanone is the precursor to methyl ethyl ketone peroxide, which is a catalyst for some polymerization reactions such as crosslinking of unsaturated polyester resins. Dimethylglyoxime can be prepared from butanone first by reaction with ethyl nitrite to give diacetyl monoxime followed by conversion to the dioxime:[15]

As of 2010[update], the United States Environmental Protection Agency (EPA) listed butanone as a toxic chemical. There are reports of neuropsychological effects. It is rapidly absorbed through undamaged skin and lungs. It contributes to the formation of ground-level ozone, which is toxic in low concentrations.[16]

Emission of butanone was regulated in the US as a hazardous air pollutant, because it is a volatile organic compound contributing to the formation of tropospheric (ground-level) ozone. In 2005, the US Environmental Protection Agency removed butanone from the list of hazardous air pollutants (HAPs).[22][23][24]

The memory of experiences and learned information is critical for organisms to make choices that aid their survival. C. elegans navigates its environment through neuron-specific detection of food and chemical odors, and can associate nutritive states with chemical odors, temperature, and the pathogenicity of a food source. Here, we describe assays of C. elegans associative learning and short- and long-term associative memory. We modified an aversive olfactory learning paradigm to instead produce a positive response; the assay involves starving 400 worms, then feeding the worms in the presence of the AWC neuron-sensed volatile chemoattractant butanone at a concentration that elicits a low chemotactic index (similar to Toroyama et al.). A standard population chemotaxis assay1 tests the worms' attraction to the odorant immediately or minutes to hours after conditioning. After conditioning, wild-type animals' chemotaxis to butanone increases 0.6 Chemotaxis Index units, its "Learning Index". Associative learning is dependent on the presence of both food and butanone during training. Pairing food and butanone for a single conditioning period ("massed training") produces short-term associative memory that lasts 2 hours. Multiple conditioning periods with rest periods between ("spaced training") yields long-term associative memory (

The first mutant with defects in butanone enhancement, olrn-1, had a mutation in the gene encoding a novel transmembrane protein [Torayama et al. (2007), their Fig.4 ( )]. olrn-1 expression was restricted to head and pharyngeal neurons, and its expression in AWC was strictly required for proper butanone enhancement. In olrn-1, the odorant receptor STR-2 was not expressed in AWC neurons (2AWCOFF). A 2AWCOFF phenotype could result from a structural deficiency in AWC, leading to a nonspecific cellular defect, or an alteration in AWC receptor distribution. Because olrn-1 mutants sensed butanone and benzaldehyde, which are detected exclusively by AWC neurons, the second possibility is more likely. In this context, the authors examined the relationship of olrn-1 with genes related to AWCON/OFF determination fate such as nsy-1 [homolog of the human MAPKKK (mitogen-activated protein kinase kinase kinase) ASK-1] (Bargmann, 2006). nsy-1 expressed STR-2 in both AWC neurons (2AWCON) and showed normal butanone enhancement. nsy-1 mutation is epistatic to olrn-1, which means that olrn-1 functions upstream of nsy-1 in AWCON/OFF determination and butanone plasticity [Torayama et al. (2007), their Fig.5 ( )].

Torayama et al. (2007) report that a series of mutants with 2AWCOFF phenotype, or AWCON surgically ablated wild-type animals, consistently had defects on butanone olfactory learning. In contrast, mutants with 2AWCON neurons had normal butanone enhancement. These results suggest that at least one functional AWCON neuron is required for butanone enhancement. However, AWCOFF is necessary for odor discrimination (Bargmann, 2006). Therefore, AWC left/right asymmetry seems to be significant for the contrast of different olfactory cues.

We have been studying behavioral plasticity induced by AWC-sensed odorants and food. AWC neurons are bilateral ciliated olfactory neurons in the head that sense butanone, benzaldehyde, isoamyl alcohol, 2,3-pentanedione, etc. (Bargmann et al., 1993). The two AWC neurons look similar in structure but are different in the expression of the G-protein-coupled receptor STR-2, which is randomly expressed in either the left or the right AWC neuron but never in both (Troemel et al., 1999; Sagasti et al., 2001). The asymmetry is initiated by axon contact between the two AWC neurons, followed by the repression of calcium signaling and the NSY-1/ASK1 MAPKKK (mitogen-activated protein kinase kinase kinase) signaling in only one of them, in which STR-2 is expressed. The DAF-11 and ODR-1 guanylyl cyclases are required to maintain the STR-2 expression. There are also functional differences between the two AWC neurons: low concentrations of butanone can be detected only by the STR-2-expressing (AWCON) neuron, whereas low concentrations of 2,3-pentanedione only by the STR-2 nonexpressing (AWCOFF) neuron (Wes and Bargmann, 2001).

The assay of butanone enhancement was based on the standard assay for adaptation (Colbert and Bargmann, 1995). Animals were washed twice with S basal and once with distilled water and transferred to a 9 cm plate containing 10 ml of NGM agar with or without E. coli OP50 (food) for preexposure. The agar contained 5 mm serotonin (Creatinine Sulfate Complex; Sigma, St. Louis, MO) when the effect of exogenous serotonin was tested. Odorant was distributed among six agar plugs on the lid of the plate, and the plate was sealed with Parafilm. After preexposure for 90 min, the animals were washed twice with S basal and once with distilled water and tested for the chemotaxis assay or the selection assay as described above. The amounts of odorants used for the preexposure were 12 μl in butanone enhancement, 30 μl in the butanone adaptation, 1.8 μl in benzaldehyde adaptation, and 12 μl in isoamyl alcohol adaptation.

The duration of the memory of preexposure was investigated by changing the length of the interval between the end of preexposure and the start of chemotaxis (Fig. 2A). When the animals were kept in the absence of butanone and food during the interval, the memory lasted for 4 h but not 8 h (Fig. 2B). In contrast, when animals were kept in the absence of butanone but presence of food, the chemotaxis index decreased more quickly (in 1 h) to the level of naive animals (Fig. 2C). This may be interpreted as a kind of unlearning or dissociation of butanone and food signals. In the presence of butanone but absence of food, the chemotaxis index fell off in 30 min to a very low level as a result of adaptation to butanone (Fig. 2C). The memory (>4 h) seems to be kept longer than other memories of smell, taste, or temperature (Colbert and Bargmann, 1995, 1997; Gomez et al., 2001; Saeki et al., 2001; Mohri et al., 2005), except the memory of olfactory imprinting (Remy and Hobert, 2005), which lasts for a lifetime but can be gained only at the L1 larval stage.

Using the selection assay after preexposure to butanone and food (see Materials and Methods), we isolated 10 mutants that showed abnormality in butanone enhancement and named them olrn (olfactory learning) mutants. Two of them, olrn-1(ut305) and olrn-2(ut306), which showed the strongest abnormality among these mutants, were characterized further. Without preexposure, both olrn-1 and olrn-2 animals exhibited normal chemotaxis to 1:10 butanone (Fig. 3A). After exposure to butanone in the absence of food, they showed normal adaptation to butanone. However, after exposure to butanone in the presence of food, the mutants did not increase but decreased their response to butanone, as if they had defects in the sensation of food, integration of the signals of butanone and food, or formation of the memory. In the selection assay, they migrated to the control odorant even after exposure to butanone and food, as expected.

Cloning and expression of olrn-1 gene and cell-specific rescue of the olrn-1(ut305) butanone enhancement phenotype. A, Genetic map, physical map, and genomic rescue experiments. The bottom indicates the regions of the genome used for rescue experiments as well as the results of rescue experiments. B, Predicted amino acid sequence of OLRN-1 (a- and b-type). Predicted transmembrane domains and the region showing homology to Drosophila Raw are shown, together with a partial amino acid sequence of Raw. C, Rescue of the butanone (But) enhancement defect of olrn-1 with the wild type olrn-1 cDNA driven by a variety of cell-specific promoters. The selection assay was used to detect the rescue sensitively. The left two columns show control experiments with wild-type and olrn-1(ut305) animals. The olrn-1 cDNA driven by the H20 (pan-neuronal), gcy-10 (AWC, AWB, and I1), and odr-3 (AWC, AWA, AWB, ASH, and ADF) promoters, but not str-1 (AWB), str-2 (AWCON), or ttx-3 (AIY) promoters, rescued all of the olrn-1 mutant phenotypes. Four to six plates were used for all data. *p

Bardet-Biedl syndrome genes are required for butanone enhancement in AWCON neurons, whereas other cilium structure genes are not required. A, Rescue of the olrn-2 butanone enhancement phenotype with the wild-type olrn-2 cDNA driven by str-2 (AWCON) and gcy-10 (AWB and AWC) promoters. Results of three independent lines of animals carrying extrachromosomal array are shown for each promoter. The selection assay was used to detect the rescue sensitively. Four to six plates were used for all data. *p B, Mutants in Bardet-Biedl syndrome genes exhibited defects in butanone enhancement. olrn-2(ut306) is allelic to bbs-8(nx77), and osm-12 gene encodes the C. elegans BBS-7. Four to 15 plates were used for all data. C, Mutants in other cilium structure genes did not exhibit defects in butanone enhancement. gpa-3(gf) is a strain with a chromosomal insertion of the gain-of-function (Q205L) mutant gpa-3 transgenes. Four to 15 plates were used for all data. The error bars indicate SEM. 041b061a72


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