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Biology subjects

Bradford, E. F.

Publications and source records attributed to Bradford, E. F..

2 recordsLinked to original sources

Post-biting behavioral reprogramming underlies reproductive efficiency in Aedes aegypti mosquitoes

The global spread and increasing populations of disease vector mosquitoes expose hundreds of millions of people to mosquito-borne illnesses each year. Female Aedes aegypti mosquitoes, global vectors of dengue, require protein from host blood to support egg development and undergo repeated cycles of blood-feeding and egg-laying. After biting, females temporarily alter their behavioral state and suppress host-seeking while using blood-derived nutrients to develop eggs. Host-seeking suppression ends once eggs are laid. While this period has generally been thought of as one of behavioral inactivity, we reveal that it instead reflects behavioral reprogramming, during which females transition from post-blood-meal inactivity into active searching for egglaying sites. Females with mature eggs show a distinct behavioral state characterized by increased locomotor activity and a shift in circadian behavioral timing, leading to nocturnal humidity-seeking and egg-laying in an otherwise diurnal species. We show that the circadian clock gene cycle is critical for regulating this transition; its absence disrupts the timing of oviposition behaviors, leading to poor site selection and reduced predicted offspring survival. These findings suggest that during egg development, circadian clock-dependent behavioral reprogramming triggers nocturnal hyperactivity and oviposition site search, an essential process for mosquito reproduction and population viability.

neuroscience↗

Widespread employment of conserved C. elegans homeobox genes in neuronal identity specification

Homeobox genes are prominent regulators of neuronal identity, but the extent to which their function has been probed in animal nervous systems remains limited. In the nematode Caenorhabditis elegans, each individual neuron class is defined by the expression of unique combinations of homeobox genes, prompting the question of whether each neuron class indeed requires a homeobox gene for its proper identity specification. We present here progress in addressing this question by extending previous mutant analysis of homeobox gene family members and describing multiple examples of homeobox gene function in different parts of the C. elegans nervous system. To probe homeobox function, we make use of a number of reporter gene tools, including a novel multicolor reporter transgene, NeuroPAL, which permits simultaneous monitoring of the execution of multiple differentiation programs throughout the entire nervous system. Using these tools, we add to the previous characterization of homeobox gene function by identifying neuronal differentiation defects for 12 homeobox genes in 20 distinct neuron classes that are mostly unrelated by location, function and lineage history. 10 of these 20 neuron classes had no homeobox gene function ascribed to them before, while in the other 10 neuron classes, we extend the combinatorial code of transcription factors required for specifying terminal differentiation programs. Furthermore, we demonstrate that in a particular lineage, homeotic identity transformations occur upon loss of a homeobox gene and we show that these transformations are the result of changes in homeobox codes. Combining the present with past analysis, 111 of the 118 neuron classes of C. elegans are now known to require a homeobox gene for proper execution of terminal differentiation programs. Such broad deployment indicates that homeobox function in neuronal identity specification may be an ancestral feature of animal nervous systems.

neuroscience↗