A Balbiani body and the fusome mediate mitochondrial inheritance during<i>Drosophila</i>oogenesis

Cox, Rachel T.; Spradling, Allan C.

doi:10.1242/dev.00365

Cited by 296 publications

(330 citation statements)

References 55 publications

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“…A similar mutant in Caenorhabditis elegans kinesin-1, uncoordinated-116 (unc-116), also did not affect organelle transport (20). To test the ability of this mutant to transport cargoes in the germline, we assayed the distribution of mitochondria, well-known kinesin-1-dependent organelles (3), using a mitochondrial EGFP marker (21). We found that mitochondria were distributed correctly in stage 1-3 egg chambers of Khc mutA oocytes (Fig.…”

Section: Resultsmentioning

confidence: 97%

Microtubule–microtubule sliding by kinesin-1 is essential for normal cytoplasmic streaming in Drosophila oocytes

Lü

Winding

Lakonishok

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

122

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Cytoplasmic streaming in Drosophila oocytes is a microtubulebased bulk cytoplasmic movement. Streaming efficiently circulates and localizes mRNAs and proteins deposited by the nurse cells across the oocyte. This movement is driven by kinesin-1, a major microtubule motor. Recently, we have shown that kinesin-1 heavy chain (KHC) can transport one microtubule on another microtubule, thus driving microtubule-microtubule sliding in multiple cell types. To study the role of microtubule sliding in oocyte cytoplasmic streaming, we used a Khc mutant that is deficient in microtubule sliding but able to transport a majority of cargoes. We demonstrated that streaming is reduced by genomic replacement of wild-type Khc with this sliding-deficient mutant. Streaming can be fully rescued by wild-type KHC and partially rescued by a chimeric motor that cannot move organelles but is active in microtubule sliding. Consistent with these data, we identified two populations of microtubules in fast-streaming oocytes: a network of stable microtubules anchored to the actin cortex and free cytoplasmic microtubules that moved in the ooplasm. We further demonstrated that the reduced streaming in sliding-deficient oocytes resulted in posterior determination defects. Together, we propose that kinesin-1 slides free cytoplasmic microtubules against cortically immobilized microtubules, generating forces that contribute to cytoplasmic streaming and are essential for the refinement of posterior determinants.kinesin-1 | microtubules | cytoplasmic streaming | Drosophila | axis determination

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Section: Resultsmentioning

confidence: 97%

Microtubule–microtubule sliding by kinesin-1 is essential for normal cytoplasmic streaming in Drosophila oocytes

Lü

Winding

Lakonishok

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

122

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“…The CFP and YFP fluorescence patterns were mitochondrial, and in live egg chambers the signals moved as mitochondria did 26 (data not shown). In nosCIETDY egg chambers, the CFP and YFP signals overlapped completely (Figures 2a, lower egg chamber, and b, white color) when there was no evidence of apoptosis.…”

Section: Detection Of In Vivo Caspase Activitymentioning

confidence: 94%

Illuminating the role of caspases during Drosophila oogenesis

Mazzalupo

Cooley

2006

Cell Death Differ

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Cell death is a prominent feature of animal germline development. In Drosophila, the death of 15 nurse cells is linked to the development of each oocyte. In addition, females respond to poor environmental conditions by inducing egg chamber death prior to yolk uptake by the oocyte. To study these two forms of cell death, we analyzed caspase activity in the germline by expressing a transgene encoding a caspase cleavage site flanked by cyan fluorescent protein and yellow fluorescent protein. When expressed in ovaries undergoing starvation-induced apoptosis, this construct was an accurate reporter of caspase activity. However, dying nurse cells at the end of normal oogenesis showed no evidence of cytoplasmic caspase activity. Furthermore, although expression of the caspase inhibitors p35 or Drosophila inhibitor of apoptosis protein 1 blocked starvation-induced death, it did not affect normal nurse cell death or overall oogenesis in well-fed females. Our data suggest that caspases play no role in developmentally programmed nurse cell death.

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“…Mitochondria form aggregates with the smooth endoplasmic reticulum (SER), Cummins et al, 1997;Cox and Spradling, 2003;Mitochondrial distribution Wilding et al, 2001Torner et al, 2004;Nishi et al, 2003Mitochondrial movement van Blerkom, 1991Cox and Spradling, 2003;mtDNA content Reynier et al, 2001Spikings et al, 2007mtDNA mutation Yesodi et al, 2002Hsieh et al, 2004Mitochondrial polarity van Blerkom et al, 2003 2007 Function in calcium regulation Machaty et al, 1997;Krisher, 2004;Whitaker, 2008 Mitochondrial dysfunction Tarín, 1996;Eichenlaub-Ritter, 1998;Yin et al, 1998;Ottolenghi et al, 2004;Thouas et al, 2004;Zhang et al, 2006Mitochondria transfer Pinkert et al, 1997Malter and Cohen, 2002;Kong et al, 2004;Yi et al, 2007 a Studies involved in oocytes and embryos and these aggregates are apparently involved in the energy production and deposition before fertilization (Torner et al, 2004). Mammalian oocyte maturation relies not only on a high level of ATP for nuclear envelope breakdown, but also on intracellular calcium, which is derived from the endoplasmic reticulum (ER) and mitochondria (Krisher, 2004).…”

Section: Calcium Signaling In Mitochondriamentioning

confidence: 99%

Mitochondrial functions on oocytes and preimplantation embryos

Wang

Zou

et al. 2009

J. Zhejiang Univ. Sci. B

135

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Oocyte quality has long been considered as a main limiting factor for in vitro fertilization (IVF). In the past decade, extensive observations demonstrated that the mitochondrion plays a vital role in the oocyte cytoplasm, for it can provide adenosine triphosphate (ATP) for fertilization and preimplantation embryo development and also act as stores of intracellular calcium and proapoptotic factors. During the oocyte maturation, mitochondria are characterized by distinct changes of their distribution pattern from being homogeneous to heterogeneous, which is correlated with the cumulus apoptosis. Oocyte quality decreases with the increasing maternal age. Recent studies have shown that low quality oocytes have some age-related dysfunctions, which include the decrease in mitochondrial membrane potential, increase of mitochondrial DNA (mtDNA) damages, chromosomal aneuploidies, the incidence of apoptosis, and changes in mitochondrial gene expression. All these dysfunctions may cause a high level of developmental retardation and arrest of preimplantation embryos. It has been suggested that these mitochondrial changes may arise from excessive reactive oxygen species (ROS) that is closely associated with the oxidative energy production or calcium overload, which may trigger permeability transition pore opening and subsequent apoptosis. Therefore, mitochondria can be seen as signs for oocyte quality evaluation, and it is possible that the oocyte quality can be improved by enhancing the physical function of mitochondria. Here we reviewed recent advances in mitochondrial functions on oocytes.

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A Balbiani body and the fusome mediate mitochondrial inheritance duringDrosophilaoogenesis

Cited by 296 publications

References 55 publications

Microtubule–microtubule sliding by kinesin-1 is essential for normal cytoplasmic streaming in Drosophila oocytes

Microtubule–microtubule sliding by kinesin-1 is essential for normal cytoplasmic streaming in Drosophila oocytes

Illuminating the role of caspases during Drosophila oogenesis

Mitochondrial functions on oocytes and preimplantation embryos

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