The Drosophila Nuclear Lamina Protein Otefin Is Required for Germline Stem Cell Survival

Barton, Lacy J.; Pinto, Belinda S.; Wallrath, Lori L.; Geyer, Pamela

doi:10.1016/j.devcel.2013.05.023

Cited by 23 publications

(70 citation statements)

References 54 publications

(67 reference statements)

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“…To determine whether Bocks contributes to nuclear lamina function in early stages of germ-cell development, we examined larval gonads. Previous studies have shown that loss of Ote reduces the number of primordial germ cells (PGCs) in the third-instar larval gonads (Barton et al 2013). To understand whether Bocks protects PGCs from Ote loss, we stained lem-d double-mutant larval gonads with antibodies against Vasa and Spectrin (Figure 7).…”

Section: Generation Of Bocks Mutantsmentioning

confidence: 99%

“…Crosses were carried out in vials at 25°, unless otherwise noted. Stocks used in this study include y 1 w 67c23 (the wild-type reference control), two dMAN1 alleles [dMAN1 D81 and dMAN1 D26 (Pinto et al 2008)], and two ote alleles [ote B279-G and ote halPk (Barton et al 2013)]. …”

Section: Drosophila Stocks and Culture Conditionsmentioning

confidence: 99%

“…Larval body wall muscles form during embryogenesis when maternally contributed LEM-D proteins are present. Thus, it remains possible that LEM-D proteins contribute to the formation of nuclear lamina in muscle nuclei.Increased expression of Bocks rescues GSC loss in ote 2/2 ovaries Loss of dMAN1 or Ote causes tissue-restricted adult phenotypes (Jiang et al 2008;Pinto et al 2008;Wagner et al 2010;Barton et al 2013). We reasoned that such phenotypes might result because of cell-specific differences in the nuclear lamina, wherein affected cells may have insufficient amounts of a compensating LEM-D protein.…”

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confidence: 99%

“…In Drosophila ovaries, GSCs reside within the germarium, a structure comprised of somatic cells niche cells and two to three GSCs (Chen et al 2011;Harris and Ashe 2011;Losick et al 2011). In young ote 2/2 females, ovaries display a complex germarial phenotype, wherein some germaria carry no germ cells, termed GSC loss, and some germaria carry more than five GSC-like cells, termed GSC expansion (Barton et al 2013). To determine the ability of other LEM-D proteins to rescue these phenotypes, ovaries obtained from ote 2/2 , P[hsp70:lem-d] heat-treated females were stained with antibodies against Vasa, a germlinespecific helicase, and Spectrin, a cytoskeletal protein that localizes to the cytoplasmic periphery in somatic cells and forms a spherical structure called the spectrosome in GSCs (Lin et al 1994).…”

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confidence: 99%

“…Loss of dMAN1 causes a moderate decrease in adult viability, with surviving adults showing male sterility, decreased female fertility due to egg retention, defects in neuromuscular junctions, flightlessness associated with altered wing patterning and positioning, and locomotion difficulties (Pinto et al 2008;Wagner et al 2010). In contrast, phenotypes associated with ote 2/2 mutants are restricted to the ovary, where germline stem cells (GSCs) show age-enhanced loss (Jiang et al 2008;Barton et al 2013). The nonoverlapping defects associated with Ote and dMAN1 loss imply that these proteins make unique regulatory contributions during development.…”

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confidence: 99%

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Unique and Shared Functions of Nuclear Lamina LEM Domain Proteins in Drosophila

et al. 2014

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The nuclear lamina is an extensive protein network that contributes to nuclear structure and function. LEM domain (LAP2, emerin, MAN1 domain, LEM-D) proteins are components of the nuclear lamina, identified by a shared 45-amino-acid motif that binds Barrier-to-autointegration factor (BAF), a chromatin-interacting protein. Drosophila melanogaster has three nuclear lamina LEM-D proteins, named Otefin (Ote), Bocksbeutel (Bocks), and dMAN1. Although these LEM-D proteins are globally expressed, loss of either Ote or dMAN1 causes tissue-specific defects in adult flies that differ from each other. The reason for such distinct tissue-restricted defects is unknown. Here, we generated null alleles of bocks, finding that loss of Bocks causes no overt adult phenotypes. Next, we defined phenotypes associated with lem-d double mutants. Although the absence of individual LEM-D proteins does not affect viability, loss of any two proteins causes lethality. Mutant phenotypes displayed by lem-d double mutants differ from baf mutants, suggesting that BAF function is retained in animals with a single nuclear lamina LEM-D protein. Interestingly, lem-d double mutants displayed distinct developmental and cellular mutant phenotypes, suggesting that Drosophila LEM-D proteins have developmental functions that are differentially shared with other LEM-D family members. This conclusion is supported by studies showing that ectopically produced LEM-D proteins have distinct capacities to rescue the tissue-specific phenotypes found in single lem-d mutants.Our findings predict that cell-specific mutant phenotypes caused by loss of LEM-D proteins reflect both the constellation of LEM-D proteins within the nuclear lamina and the capacity of functional compensation of the remaining LEM-D proteins. T HE nuclear lamina is an extensive protein network underlying the nuclear envelope. This network is composed of the nucleus-specific intermediate filament proteins, the Aand B-type lamins, which form a structural platform for association of .200 proteins (Schirmer et al. 2003;Korfali et al. 2010;Malik et al. 2010). LEM domain (LAP2, emerin, MAN1 domain, LEM-D) proteins represent one family of lamin interacting proteins. This family shares an 45-residue bihelical domain that was first identified in LAP2, emerin, and MAN1 (Lin et al. 2000;Mansharamani and Wilson 2005;Wagner and Krohne 2007). LEM-D proteins interact with the small, conserved protein called Barrier-to-autointegration factor (BAF), a protein that binds double-strand DNA and histones (Zheng et al. 2000;Cai et al. 2001;Laguri et al. 2001;Furukawa et al. 2003;Liu et al. 2003;Montes de Oca et al. 2005). Through interactions with BAF, LEM-D proteins connect interphase chromosomes to the nuclear lamina, thereby contributing to global nuclear organization.Metazoan genomes encode several LEM-D proteins (Lee and Wilson 2004;Berk et al. 2013). Most show enriched localization within the nuclear lamina, wherein the LEM-D proteins direct shared protein associations. For example, emerin and MAN1 in...

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Section: Generation Of Bocks Mutantsmentioning

confidence: 99%

Section: Drosophila Stocks and Culture Conditionsmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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