Project description: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 lov(47) , Lov expression is lost in many embryonic neurons including the two lateral chordotonal neurons. lov(47) mutant larvae show feeding and locomotor defects including spontaneous backward movement. Adult lov(47) males perform aberrant courtship behavior distinguished by courtship displays that are not directed at the female. lov(47) adults also show more defective negative gravitaxis than the previously isolated lov(91Y) mutant. In contrast, lov(66) 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 lov(66) .

Project description:In the U.S., Black adults consistently have higher allostatic load – an indicator of physiological dysregulation – than White adults. Education is considered a likely mechanism given racial differences in attainment, but evidence is mixed. This may be due, in part, to data limitations that have made it difficult for scholars to account for the structurally rooted systemic racism that shaped the U.S. education system and led to large racial inequities in school term length and school attendance among older adults who grew up in the Jim Crow South. Our study addresses this limitation by linking historical data on Black and White segregated school systems in the U.S. South from 1919 to 1954 to the Health and Retirement Study (HRS) to determine if a new measure of educational attainment that accounts for structural racism that led to differences in the number of school days attended by Black and White students across years and states better explains Black-White inequities in allostatic load among older adults who attended school during Jim Crow. We restrict our sample to HRS respondents racialized as White or Black, who resided in the South when they were school-aged, completed primary/secondary school between 1919 and 1954, and provided a measure of allostatic load (n = 1932). We find that our new measure of schooling – duration in school – reduced the Black-White inequity in allostatic load more so than self-reported years of schooling whether we measured allostatic load continuously (34% vs 16%) or categorically (45% vs 20%). Our findings highlight the importance of identifying and using historically informed measures of schooling that account for structurally rooted systemic racism when trying to understand how education shapes the health of individuals racialized as Black in the United States. Highlights • U.S. Black adults show greater physiological dysregulation than White adults.• Mixed evidence as to whether education explains this inequity.• May be due to unmeasured structurally rooted systematic racism in early schooling.• Our education measure accounts for race inequity in term length and days attended.• This measure explains Black-White inequity in allostatic load.

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Jim McSherry

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