Cell-specific expression of the lark RNA-binding protein in Drosophila results in morphological and circadian behavioral phenotypes.

Dec 12, 2003Journal of neurogenetics

Effects of the lark RNA-binding protein in specific fruit fly cells on body shape and daily activity patterns

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Abstract

LARK expression in Crustacean Cardioactive Peptide (CCAP) neurons caused an early-eclosion phenotype.

Increasing LARK levels in Eclosion Hormone (EH) cells resulted in abnormally late peaks of eclosion.
LARK expression in Pigment Dispersing Factor (PDF)- or TIMELESS (TIM)-containing clock neurons led to behavioral arrhythmicity despite normal clock protein cycling.
The effects of LARK expression were similar to those observed with genetic removal of the relevant peptidergic populations, indicating a functional alteration rather than cell death.
Reduced PDF immunoreactivity in PDF neurons expressing LARK suggests possible disruption in neuropeptide synthesis, transport, or release.
LARK expression in other cell types did not show significant effects on development, viability, or behavior, indicating specificity in its action.

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Past studies have implicated the Drosophila LARK protein in the circadian control of adult eclosion behavior. LARK has a broad tissue pattern of distribution, and is pan-neuronal in the differentiated brain. In certain peptidergic neurons, LARK abundance changes in a circadian manner. However, the precise cellular requirement for LARK, with respect to circadian behavior, is still not known. To explore this issue, we employed the GAL4/UAS binary expression system to increase LARK abundance in defined neuronal cell types. Interestingly, LARK expression in Crustacean Cardioactive Peptide (CCAP) neurons caused an early-eclosion phenotype, whereas a similar perturbation in the Eclosion Hormone (EH) cells resulted in abnormally late peaks of eclosion. Surprisingly, LARK expression in Pigment Dispersing Factor (PDF)- or TIMELESS (TIM)-containing clock neurons caused behavioral arrhythmicity, even though clock protein cycling was found to be normal in these flies. Although the observed effects of LARK expression mirrored those seen with genetic ablation of the relevant peptidergic populations, there was no evidence of defective cell development or morphology. This suggests that an alteration of cell function rather than cell death is the cause of the aberrant phenotypes. Diminished PDF immunoreactivity in flies expressing LARK in the PDF neurons suggests that an effect on neuropeptide synthesis, transport, or release may contribute to the observed arrhythmicity. Importantly, the expression of LARK in several other cell populations did not have detectable effects on development, viability or behavior, indicating a specificity of action within certain cell types.

Cell-specific expression of the lark RNA-binding protein in Drosophila results in morphological and circadian behavioral phenotypes.

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