Biology subjects

Marenda, D. R.

Publications and source records attributed to Marenda, D. R..

4 recordsLinked to original sources

bioRxiv2019

Extramacrochaete promotes branch and bouton number via the sequestration of Daughterless in the cytoplasm of neurons.

The class I basic Helix Loop Helix (bHLH) proteins are highly conserved transcription factors that are ubiquitously expressed. A wealth of literature on class I bHLH proteins have shown that these proteins must homodimerize or heterodimerize with tissue specific HLH proteins in order to bind DNA at E box (CANNTG) consensus sequences to control tissue specific transcription. Due to its ubiquitous expression, class I bHLH proteins are also extensively regulated post-translationally, mostly through dimerization. Previously, we reported that in addition to its role in promoting neurogenesis, the class I bHLH protein Daughterless also functions in mature neurons to restrict axon branching and synapse number. Here, we show that part of the molecular logic that specifies how Daughterless functions in neurogenesis is also conserved in neurons. We show that the type V HLH protein Extramacrochaete binds to and represses Daughterless function by sequestering Daughterless to the cytoplasm. This work provides initial insights into the mechanisms underlying the function of Daughterless and Extramacrochatae in neurons while providing a novel understanding of how Extramacrochaetae functions to restricts Daughterless activity within the cell.

neuroscience↗

bioRxiv2019

Larval mannitol diets increase mortality, prolong development, and decrease adult body sizes in fruit flies (Drosophila melanogaster).

Ingestion of the polyol mannitol caused sex-biased mortality in adult Drosophila melanogaster, but larval mortality was not sex-biased. High-sugar diets prolong development and generate smaller adult body sizes in D. melanogaster. We hypothesized that mannitol ingestion would generate similar developmental phenotypes as other high-carbohydrate diets. We predicted concentration-dependent effects on development similar to high-sugar diets when D. melanogaster larvae are fed mannitol, as well as a concentration-dependent amelioration of developmental effects if introduction to mannitol media is delayed past the third instar. Both male and female larvae had prolonged development and smaller adult body sizes when fed increasing concentrations of mannitol. Mannitol-induced increases in mortality were concentration dependent in 0 M to 0.8 M treatments beginning as early as 48 hours post-hatching. Larval survival, and pupation and eclosion times, were normal in 0.4 M mannitol treatments when larvae were first introduced to mannitol 72 hours post-hatching (the beginning of the third-instar); the adverse mannitol effects occurred in 0.8 M mannitol treatments, but at a lower magnitude. Female D. melanogaster adults prefer laying eggs on diets with high sugar concentrations, despite the negative effects on offspring performance. However, when given a choice, female D. melanogaster avoided laying eggs on mannitol-containing media that was otherwise identical to the control media, suggesting females perceived and avoided mannitol. In conclusion, the developmental effects of a larval mannitol diet closely resemble those of high-sugar diets, but adult female oviposition responses to mannitol in laying substrates are distinct from responses to other carbohydrates.

zoology↗

bioRxiv2019

Mannitol ingestion causes concentration-dependent, sex-specific mortality in adults of the fruit fly (Drosophila melanogaster).

Mannitol, a sugar alcohol used in commercial food products, induced sex-specific mortality in the fruit fly Drosophila melanogaster when ingested at a single concentration (1M), and female mortality was greater than male mortality. We hypothesized that sex differences in energy needs, related to reproductive costs, contribute to increased mortality in females compared to males. To test for the effects of reproductive costs, we compared longevity to 21 days of actively mating and non-mating flies fed various concentrations of mannitol. We also asked whether mannitol-induced mortality was concentration-dependent for both males and females, and if mannitols sex-specific effects were consistent across concentrations. Females and males both showed concentration-dependent increases in mortality, but female mortality was consistently higher at all concentrations above 0.75M. Fly longevity to 21 days decreased further for both sexes when housed in mixed sex vials (as compared to single sex vials), suggesting the increased energetic demands of reproduction for both sexes may increase ingestion of mannitol. Mannitol fed to larvae did not alter emerging adult sex ratios, suggesting that sex-specific mortality due to mannitol occurs only in adults.

zoology↗

bioRxiv2018

The Drosophila chromodomain protein Kismet activates steroid hormone receptor transcription to govern axon pruning and memory in vivo.

Axon pruning is critical for the proper synapse elimination required for sculpting precise neural circuits. Though axon pruning has been described in the literature for decades, relatively little is known about the molecular and cellular mechanisms that govern axon pruning in vivo. Here, we show that the epigenetic reader Kismet (Kis) binds to cisregulatory elements of the steroid hormone receptor Ecdysone Receptor (EcR) gene in Drosophila neurons. Kis is required to activate EcR transcription at these elements and promote H3K36 di- and tri-methylation and H4K16 acetylation. We show that exogenous EcR can rescue axon pruning and memory defects associated with loss of Kis, and that the histone deacetylase inhibitor SAHA can rescue these phenotypes. EcR protein abundance is a cell-autonomous, rate-limiting step required to initiate axon pruning in Drosophila, and our data suggests that this step is under epigenetic control.\n\nHighlights (bullet points up to 4)O_LIThe chromodomain reader Kismet activates transcription of the steroid hormone receptor EcR-B1 in the Drosophila to initiate developmental axon pruning.\nC_LIO_LIKismet promotes H3K36 di- and tri-methylation and H4K16 acetylation at the EcR locus and upstream cis-regulatory sites.\nC_LIO_LIAxon pruning and memory defects associated with loss of Kismet are significantly rescued by general HDAC inhibition.\nC_LI

neuroscience↗