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Start Over Author "White, Benjamin H." Journal genetics
7 results on '"White, Benjamin H."'

5. The Splice Isoforms of the Drosophila Ecdysis Triggering Hormone Receptor Have Developmentally Distinct Roles.

Author

Diao, Feici, Mena, Wilson, Shi, Jonathan, Dongkook Park, Fengqiu Diao, Taghert, Paul, Ewer, John, and White, Benjamin H.

Subjects
*RNA splicing, *DROSOPHILA genetics, *ECDYSIS, *HORMONE receptors, *ANIMAL exoskeletons, *ENDOCRINE diseases, *GENETICS
Abstract

To grow, insects must periodically shed their exoskeletons. This process, called ecdysis, is initiated by the endocrine release of Ecdysis Trigger Hormone (ETH) and has been extensively studied as a model for understanding the hormonal control of behavior. Understanding how ETH regulates ecdysis behavior, however, has been impeded by limited knowledge of the hormone's neuronal targets. An alternatively spliced gene encoding a G-protein-coupled receptor (ETHR) that is activated by ETH has been identified, and several lines of evidence support a role in ecdysis for its A-isoform. The function of a second ETHR isoform (ETHRB) remains unknown. Here we use the recently introduced "Trojan exon" technique to simultaneously mutate the ETHR gene and gain genetic access to the neurons that express its two isoforms. We show that ETHRA and ETHRB are expressed in largely distinct subsets of neurons and that ETHRA- but not ETHRB-expressing neurons are required for ecdysis at all developmental stages. However, both genetic and neuronal manipulations indicate an essential role for ETHRB at pupal and adult, but not larval, ecdysis. We also identify several functionally important subsets of ETHR-expressing neurons including one that coexpresses the peptide Leucokinin and regulates fluid balance to facilitate ecdysis at the pupal stage. The general strategy presented here of using a receptor gene as an entry point for genetic and neuronal manipulations should be useful in establishing patterns of functional connectivity in other hormonally regulated networks. [ABSTRACT FROM AUTHOR]

Published
2016
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6. Focusing Transgene Expression in Drosophila by Coupling Gal4 With a Novel Split-LexA Expression System.

Author

Chun-Yuan Ting, Gu, Stephanie, Guttikonda, Sudha, Tzu-Yang Lin, White, Benjamin H., and Chi-Hon Lee

Subjects
*DNA-binding proteins, *MOIETIES (Chemistry), *PROMOTERS (Genetics), *GENETICS, *GENE expression
Abstract

Here we report the development of a ternary version of the LexA::VP16/LexAop system in which the DNA-binding and trans-activating moieties are independently targeted using distinct promoters to achieve highly restricted, intersectional expression patterns. This Split LexA system can be concatenated with the Gal4/upstream activating sequence system to refine the expression patterns of existing Gal4 lines with minimal genetic manipulations. [ABSTRACT FROM AUTHOR]

Published
2011
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7. Facilitating Neuron-Specific Genetic Manipulations in Drosophila melanogaster Using a Split GAL4 Repressor

Author

Marta Zlatic, Michael-John Dolan, Haojiang Luan, Gregory S.X.E. Jefferis, William C. Shropshire, Robert L. Scott, Ben Sutcliffe, Benjamin T. Cocanougher, Benjamin H. White, Shahar Frechter, Jefferis, Gregory SXE [0000-0002-0587-9355], White, Benjamin H [0000-0003-0612-8075], and Apollo - University of Cambridge Repository

Subjects
0301 basic medicine, GAL4/UAS system, Zipper, 03 medical and health sciences, Upstream activating sequence, Genetics, Biological neural network, Animals, Drosophila Proteins, Gal4-UAS, Enhancer, neural circuits, Neurons, LexA-LexAop, biology, fungi, Gene Expression Regulation, Developmental, biology.organism_classification, DNA-Binding Proteins, Repressor Proteins, 030104 developmental biology, Drosophila melanogaster, Drosophila, Repressor lexA, transgene expression, Drosophila Protein, Transcription Factors
Abstract

Efforts to map neural circuits have been galvanized by the development of genetic technologies that permit the manipulation of targeted sets of neurons in the brains of freely behaving animals. The success of these efforts relies on the experimenter’s ability to target arbitrarily small subsets of neurons for manipulation, but such specificity of targeting cannot routinely be achieved using existing methods. In Drosophila melanogaster, a widely-used technique for refined cell type-specific manipulation is the Split GAL4 system, which augments the targeting specificity of the binary GAL4-UAS (Upstream Activating Sequence) system by making GAL4 transcriptional activity contingent upon two enhancers, rather than one. To permit more refined targeting, we introduce here the “Killer Zipper” (KZip+), a suppressor that makes Split GAL4 targeting contingent upon a third enhancer. KZip+ acts by disrupting both the formation and activity of Split GAL4 heterodimers, and we show how this added layer of control can be used to selectively remove unwanted cells from a Split GAL4 expression pattern or to subtract neurons of interest from a pattern to determine their requirement in generating a given phenotype. To facilitate application of the KZip+ technology, we have developed a versatile set of LexAop-KZip+ fly lines that can be used directly with the large number of LexA driver lines with known expression patterns. KZip+ significantly sharpens the precision of neuronal genetic control available in Drosophila and may be extended to other organisms where Split GAL4-like systems are used.

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