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A Caenorhabditis elegans locomotion phenotype caused by transgenic repeats of the hlh-17 promoter sequence.

ABSTRACT: Transgene technology is one of the most heavily relied upon tools in modern biological research. Expression of an exogenous gene within cells, for research and therapeutic applications, nearly always includes promoters and other regulatory sequences. We found that repeats of a non-protein coding transgenic sequence produced profound changes to the behavior of the nematode Caenorhabditis elegans. These changes were produced by a glial promoter sequence but, unexpectedly, major deficits were observed specifically in backward locomotion, a neuron-driven behavior. We also present evidence that this behavioral phenotype is transpromoter copy number-dependent and manifests early in development and is maintained into adulthood of the worm.

SUBMITTER: Stout RF

PROVIDER: S-EPMC3842965 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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A Caenorhabditis elegans locomotion phenotype caused by transgenic repeats of the hlh-17 promoter sequence.

Stout Randy F RF Grubišić Vladimir V Parpura Vladimir V

PloS one 20131128 11

Transgene technology is one of the most heavily relied upon tools in modern biological research. Expression of an exogenous gene within cells, for research and therapeutic applications, nearly always includes promoters and other regulatory sequences. We found that repeats of a non-protein coding transgenic sequence produced profound changes to the behavior of the nematode Caenorhabditis elegans. These changes were produced by a glial promoter sequence but, unexpectedly, major deficits were obser ...[more]

PMID: 24312354

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Project description:The Caenorhabditis elegans E protein ortholog HLH-2 is required for the specification and function of the anchor cell, a unique, terminally differentiated somatic gonad cell that organizes uterine and vulval development. Initially, 4 cells-2 α cells and their sisters, the β cells-have the potential to be the sole anchor cell. The β cells rapidly lose anchor cell potential and invariably become ventral uterine precursor cells, while the 2 α cells interact via LIN-12/Notch to resolve which will be the anchor cell and which will become another ventral uterine precursor cell. HLH-2 protein stability is dynamically regulated in cells with anchor cell potential; initially present in all 4 cells, HLH-2 is degraded in presumptive ventral uterine precursor cells while remaining stable in the anchor cell. Here, we demonstrate that stability of HLH-2 protein is regulated by the activity of lin-12/Notch in both α and β cells. Our analysis provides evidence that activation of LIN-12 promotes degradation of HLH-2 as part of a negative feedback loop during the anchor cell/ventral uterine precursor cell decision by the α cells, and that absence of lin-12 activity in β cells increases HLH-2 stability and may account for their propensity to adopt the anchor cell fate in a lin-12 null background. We also performed an RNA interference screen of 232 ubiquitin-related genes and identified 7 genes that contribute to HLH-2 degradation in ventral uterine precursor cells; however, stabilizing HLH-2 by depleting ubiquitin ligases in a lin-12(+) background does not result in supernumerary anchor cells, suggesting that LIN-12 activation does not oppose hlh-2 activity solely by causing HLH-2 protein degradation. Finally, we provide evidence for lin-12-independent transcriptional regulation of hlh-2 in β cells that correlates with known differences in POP-1/TCF levels and anchor cell potential between α and β cells. Together, our results indicate that hlh-2 activity is regulated at multiple levels to restrict the anchor cell fate to a single cell.

Dataset Information

A Caenorhabditis elegans locomotion phenotype caused by transgenic repeats of the hlh-17 promoter sequence.

Publications

A Caenorhabditis elegans locomotion phenotype caused by transgenic repeats of the hlh-17 promoter sequence.

Similar Datasets

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