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Bitter taste receptors confer diverse functions to neurons.

Delventhal R, Carlson JR - Elife (2016)

Bottom Line: Expression of individual Grs conferred strikingly different effects in different neurons.The results support a model in which bitter Grs interact, exhibiting competition, inhibition, or activation.The results have broad implications for the problem of how taste systems evolve to detect new environmental dangers.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, United States.

ABSTRACT
Bitter compounds elicit an aversive response. In Drosophila, bitter-sensitive taste neurons coexpress many members of the Gr family of taste receptors. However, the molecular logic of bitter signaling is unknown. We used an in vivo expression approach to analyze the logic of bitter taste signaling. Ectopic or overexpression of bitter Grs increased endogenous responses or conferred novel responses. Surprisingly, expression of Grs also suppressed many endogenous bitter responses. Conversely, deletion of an endogenous Gr led to novel responses. Expression of individual Grs conferred strikingly different effects in different neurons. The results support a model in which bitter Grs interact, exhibiting competition, inhibition, or activation. The results have broad implications for the problem of how taste systems evolve to detect new environmental dangers.

No MeSH data available.


Related in: MedlinePlus

Fluorescent confocal microscopy of whole-mount labella reveals that the ΔGr59c mutation does not cause loss of Gr59c-GAL4 expression in I-a sensilla (top two panels).The ΔGr59c mutation does not cause gain of Gr28b.a-, Gr28a-, or Gr22b-GAL4 expression in I-a sensilla (bottom six panels). (n ≥ 5 flies per genotype). White arrowheads indicate the positions of representative I-a neurons. Cell bodies of neurons that innervate I-a sensilla can be seen only in the top two panels, i.e. in Gr59c-GAL4 and ΔGr59c; Gr59c-GAL4, as indicated by white arrowheads. Full genotypes tested: Sp/CyO; Gr-GAL4/UAS-GFP and ΔGr59c; Gr-GAL4/UAS-GFP.DOI:http://dx.doi.org/10.7554/eLife.11181.014
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fig8: Fluorescent confocal microscopy of whole-mount labella reveals that the ΔGr59c mutation does not cause loss of Gr59c-GAL4 expression in I-a sensilla (top two panels).The ΔGr59c mutation does not cause gain of Gr28b.a-, Gr28a-, or Gr22b-GAL4 expression in I-a sensilla (bottom six panels). (n ≥ 5 flies per genotype). White arrowheads indicate the positions of representative I-a neurons. Cell bodies of neurons that innervate I-a sensilla can be seen only in the top two panels, i.e. in Gr59c-GAL4 and ΔGr59c; Gr59c-GAL4, as indicated by white arrowheads. Full genotypes tested: Sp/CyO; Gr-GAL4/UAS-GFP and ΔGr59c; Gr-GAL4/UAS-GFP.DOI:http://dx.doi.org/10.7554/eLife.11181.014

Mentions: We tested the expression of four Gr-GAL4 drivers, one of which is expressed in wild-type I-a sensilla but not I-b sensilla (Gr59c-GAL4), and three of which are not expressed in I-a but are expressed in I-b (Gr28a-, Gr28b.a- and Gr22b-GAL4) (Figures 1, 8; arrowheads indicate the expected positions of cell bodies of representative I-a sensilla). All drivers were tested in both △Gr59c and control backgrounds. If the I-a bitter neurons underwent a complete change in cell fate to that of I-b bitter neurons, then one would expect these neurons to lose expression of Gr59c-GAL4. This outcome was not observed (Figure 8, top two panels). In fact, expression of Gr59c-GAL4 appeared the same in the △Gr59c labellum as in the control. Likewise, none of the three drivers that are expressed in I-b were expressed in △Gr59c I-a sensilla (Figure 8, bottom six panels). These results argue against the hypothesis that I-a sensilla undergo a complete fate change switch to I-b sensilla.10.7554/eLife.11181.014Figure 8.Fluorescent confocal microscopy of whole-mount labella reveals that the ΔGr59c mutation does not cause loss of Gr59c-GAL4 expression in I-a sensilla (top two panels).


Bitter taste receptors confer diverse functions to neurons.

Delventhal R, Carlson JR - Elife (2016)

Fluorescent confocal microscopy of whole-mount labella reveals that the ΔGr59c mutation does not cause loss of Gr59c-GAL4 expression in I-a sensilla (top two panels).The ΔGr59c mutation does not cause gain of Gr28b.a-, Gr28a-, or Gr22b-GAL4 expression in I-a sensilla (bottom six panels). (n ≥ 5 flies per genotype). White arrowheads indicate the positions of representative I-a neurons. Cell bodies of neurons that innervate I-a sensilla can be seen only in the top two panels, i.e. in Gr59c-GAL4 and ΔGr59c; Gr59c-GAL4, as indicated by white arrowheads. Full genotypes tested: Sp/CyO; Gr-GAL4/UAS-GFP and ΔGr59c; Gr-GAL4/UAS-GFP.DOI:http://dx.doi.org/10.7554/eLife.11181.014
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4764594&req=5

fig8: Fluorescent confocal microscopy of whole-mount labella reveals that the ΔGr59c mutation does not cause loss of Gr59c-GAL4 expression in I-a sensilla (top two panels).The ΔGr59c mutation does not cause gain of Gr28b.a-, Gr28a-, or Gr22b-GAL4 expression in I-a sensilla (bottom six panels). (n ≥ 5 flies per genotype). White arrowheads indicate the positions of representative I-a neurons. Cell bodies of neurons that innervate I-a sensilla can be seen only in the top two panels, i.e. in Gr59c-GAL4 and ΔGr59c; Gr59c-GAL4, as indicated by white arrowheads. Full genotypes tested: Sp/CyO; Gr-GAL4/UAS-GFP and ΔGr59c; Gr-GAL4/UAS-GFP.DOI:http://dx.doi.org/10.7554/eLife.11181.014
Mentions: We tested the expression of four Gr-GAL4 drivers, one of which is expressed in wild-type I-a sensilla but not I-b sensilla (Gr59c-GAL4), and three of which are not expressed in I-a but are expressed in I-b (Gr28a-, Gr28b.a- and Gr22b-GAL4) (Figures 1, 8; arrowheads indicate the expected positions of cell bodies of representative I-a sensilla). All drivers were tested in both △Gr59c and control backgrounds. If the I-a bitter neurons underwent a complete change in cell fate to that of I-b bitter neurons, then one would expect these neurons to lose expression of Gr59c-GAL4. This outcome was not observed (Figure 8, top two panels). In fact, expression of Gr59c-GAL4 appeared the same in the △Gr59c labellum as in the control. Likewise, none of the three drivers that are expressed in I-b were expressed in △Gr59c I-a sensilla (Figure 8, bottom six panels). These results argue against the hypothesis that I-a sensilla undergo a complete fate change switch to I-b sensilla.10.7554/eLife.11181.014Figure 8.Fluorescent confocal microscopy of whole-mount labella reveals that the ΔGr59c mutation does not cause loss of Gr59c-GAL4 expression in I-a sensilla (top two panels).

Bottom Line: Expression of individual Grs conferred strikingly different effects in different neurons.The results support a model in which bitter Grs interact, exhibiting competition, inhibition, or activation.The results have broad implications for the problem of how taste systems evolve to detect new environmental dangers.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, United States.

ABSTRACT
Bitter compounds elicit an aversive response. In Drosophila, bitter-sensitive taste neurons coexpress many members of the Gr family of taste receptors. However, the molecular logic of bitter signaling is unknown. We used an in vivo expression approach to analyze the logic of bitter taste signaling. Ectopic or overexpression of bitter Grs increased endogenous responses or conferred novel responses. Surprisingly, expression of Grs also suppressed many endogenous bitter responses. Conversely, deletion of an endogenous Gr led to novel responses. Expression of individual Grs conferred strikingly different effects in different neurons. The results support a model in which bitter Grs interact, exhibiting competition, inhibition, or activation. The results have broad implications for the problem of how taste systems evolve to detect new environmental dangers.

No MeSH data available.


Related in: MedlinePlus