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Drosophila emerins control LINC complex localization and transcription to regulate myonuclear position
Author(s) -
Torrey R. Mandigo,
Blake D. Turcich,
Alyssa J. Anderson,
Michael Hussey,
Eric S. Folker
Publication year - 2019
Publication title -
journal of cell science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.384
H-Index - 278
eISSN - 1477-9137
pISSN - 0021-9533
DOI - 10.1242/jcs.235580
Subject(s) - emerin , biology , nuclear protein , inner membrane , microbiology and biotechnology , cell nucleus , lamin , genetics , nuclear localization sequence , nuclear transport , phenotype , gene , nucleus , transcription factor , mitochondrion
Mispositioned nuclei are a hallmark of skeletal muscle disease. Many of the genes that are linked to Emery-Dreifuss muscular dystrophy (EDMD) encode proteins that are critical for nuclear movement in various cells, suggesting that disruptions in nuclear movement and position may contribute to disease progression. Yet how these genes are coordinated to move nuclei is not known. Here we focused on two different emerin proteins, Bocksbeutel and Otefin and their effects on nuclear movement. Although nuclear position was dependent on both, elimination of either Bocksbeutel or Otefin produced distinct phenotypes that were based in differential effects on the KASH-domain protein Klarsicht. Specifically, loss of Bocksbeutel reduced Klarsicht localization to the nucleus and resulted in a disruption in nuclear separation. Loss of Otefin increased the transcription of Klarsicht and led to premature separation of nuclei and their positioning closer to the edge of the muscle. Consistent with opposing functions, nuclear position is normal in otefin; bocksbeutel double mutants. These data indicate emerin-dependent regulation of Klarsicht levels in the nuclear envelope are a critical determinant of nuclear position.

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