The Drosophila BTB Domain Protein Jim Lovell Has Roles in Multiple Larval and Adult Behaviors

Abstract

Innate behaviors have their origins in the specification of neural fates during development. Within Drosophila, BTB (Bric-a-brac,Tramtrack, Broad) domain proteins such as Fruitless are known to play key roles in the neural differentiation underlying such responses. We previously identified a gene, which we have termed jim lovell (lov), encoding a BTB protein with a role in gravity responses. To understand more fully the behavioral roles of this gene we have investigated its function through several approaches. Transcript and protein expression patterns have been examined and behavioral phenotypes of new lov mutations have been characterized. Lov is a nuclear protein, suggesting a role as a transcriptional regulator, as for other BTB proteins. In late embryogenesis, Lov is expressed in many CNS and PNS neurons. An examination of the PNS expression indicates that lov functions in the late specification of several classes of sensory neurons. In particular, only two of the five abdominal lateral chordotonal neurons express Lov, predicting functional variation within this highly similar group. Surprisingly, Lov is also expressed very early in embryogenesis in ways that suggests roles in morphogenetic movements, amnioserosa function and head neurogenesis. The phenotypes of two new lov mutations that delete adjacent non-coding DNA regions are strikingly different suggesting removal of different regulatory elements. In lov47, Lov expression is lost in many embryonic neurons including the two lateral chordotonal neurons. lov47 mutant larvae show feeding and locomotor defects including spontaneous backward movement. Adult lov47 males perform aberrant courtship behavior distinguished by courtship displays that are not directed at the female. lov47 adults also show more defective negative gravitaxis than the previously isolated lov91Y mutant. In contrast, lov66 produces largely normal behavior but severe female sterility associated with ectopic lov expression in the ovary. We propose a negative regulatory role for the DNA deleted in lov66.

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“…Recently it was proven that the lov gene belonged to the more closely related Ttk subgroup had roles in multiple larval and adult behaviors of Drosophila ; especially when this gene was down‐regulated, the male adults performed aberrant courtship behavior distinguished by courtship displays that were not directed at the female. In contrast, when this gene had ectopic expression in the ovary, adult females produced normal behavior but severe sterility (Bjorum et al ., ). This implied that Ttk has some roles to regulate sexual behaviors in insects.…”

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“…A loss-of-function mutant of lov demonstrates multiple behavioral defects in the larval and adult stages, including gravity sensing (Bjorum et al 2013). These behavioral defects were previously attributed to the abnormal specifications of neurons, given that an absence of lov expression in a subset of neurons in mutants of a particular lov allele was correlated with the behavioral defects (Bjorum et al 2013). The expression of lov was also observed in specific cells of the CNS midline in embryos (Wheeler et al 2008).…”

“…Therefore, in this study, we generated a deletion mutant of BobA, BobA 1 , as described below. For the lov gene, analyses using small Dfs defined the lov locus as a potential enhancer of pcx, and this possibility was confirmed using a preexisting lov mutant allele (Bjorum et al 2013).…”

“…lov encodes a Bric-a-Brac/Tramtrack/Broad/Pox virus and zinc finger (BTB/POZ) domain-containing transcription factor and is expressed in various neurons of the CNS and PNS and in the trachea during Drosophila development (Albagli et al 1995;Armstrong et al 2006). A loss-of-function mutant of lov demonstrates multiple behavioral defects in the larval and adult stages, including gravity sensing (Bjorum et al 2013). These behavioral defects were previously attributed to the abnormal specifications of neurons, given that an absence of lov expression in a subset of neurons in mutants of a particular lov allele was correlated with the behavioral defects (Bjorum et al 2013).…”

“…However, a detailed analysis of lov expression revealed that the lov gene is not a target of Notch signaling, at least in the ventral unpaired median neurons of the CNS midline (Wheeler et al 2008). Although it is still possible that lov is involved in Notch signaling activation as a component of the pathway, the contribution of lov to Notch signaling appears to be highly context-dependent, redundant, or subtle, because the defects in the cell-fate specification of neurons found in lov mutants are much milder than those of classic Notch pathway genes (Bjorum et al 2013).…”