Cellular aspects of gonadal atrophy in Drosophila P-M hybrid dysgenesis

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Cellular aspects of gonadal atrophy in Drosophila P-M hybrid dysgenesis. / Dorogova, Natalia V.; Bolobolova, Elena Us; Zakharenko, Lyudmila P.

In: Developmental Biology, Vol. 424, No. 2, 15.04.2017, p. 105-112.

Research output: Contribution to journal › Article › peer-review

Harvard

Dorogova, NV, Bolobolova, EU & Zakharenko, LP 2017, 'Cellular aspects of gonadal atrophy in Drosophila P-M hybrid dysgenesis', Developmental Biology, vol. 424, no. 2, pp. 105-112. https://doi.org/10.1016/j.ydbio.2017.02.020

APA

Dorogova, N. V., Bolobolova, E. U., & Zakharenko, L. P. (2017). Cellular aspects of gonadal atrophy in Drosophila P-M hybrid dysgenesis. Developmental Biology, 424(2), 105-112. https://doi.org/10.1016/j.ydbio.2017.02.020

Vancouver

Dorogova NV, Bolobolova EU, Zakharenko LP. Cellular aspects of gonadal atrophy in Drosophila P-M hybrid dysgenesis. Developmental Biology. 2017 Apr 15;424(2):105-112. doi: 10.1016/j.ydbio.2017.02.020

Author

Dorogova, Natalia V. ; Bolobolova, Elena Us ; Zakharenko, Lyudmila P. / Cellular aspects of gonadal atrophy in Drosophila P-M hybrid dysgenesis. In: Developmental Biology. 2017 ; Vol. 424, No. 2. pp. 105-112.

BibTeX

@article{df980016f5e3421096b353a455c98661,

title = "Cellular aspects of gonadal atrophy in Drosophila P-M hybrid dysgenesis",

abstract = "Gonadal atrophy is the most typical and dramatic manifestation of intraspecific hybrid dysgenesis syndrome leading to sterility in Drosophila melanogaster dysgenic progeny. The P-M system of hybrid dysgenesis is primarily associated with germ cell degeneration during the early stages of Drosophila embryonic development at elevated temperatures. In the present study, we have defined the phase of germ cell death as beginning at the end of embryogenesis immediately following gonad formation. However, the temperature-dependent screening of germ cell developmental patterns in the dysgenic background showed that early germ cells are susceptible to the hybrid dysgenesis at any Drosophila life-cycle stage, including in the imago. Electron microscopy of germ cells after dysgenesis induction revealed significant changes in subcellular structure, especially mitochondria, prior to cellular breakdown. The mitochondrial pathology can promote the activation of cell death pathways in dysgenic germ cells, which leads to gonadal atrophy.",

keywords = "Cell death, Drosophila, Germ cell, Hybrid dysgenesis, Oogenesis, Spermatogenesis, Germ Cells/pathology, Temperature, Mitochondria/metabolism, Male, Atrophy, Drosophila melanogaster/genetics, Phenotype, Animals, Hybridization, Genetic, Gonads/metabolism, Female, MITOCHONDRIA, DEATH, STERILITY, FEMALE, ELEMENTS, MELANOGASTER",

author = "Dorogova, {Natalia V.} and Bolobolova, {Elena Us} and Zakharenko, {Lyudmila P.}",

year = "2017",

month = apr,

day = "15",

doi = "10.1016/j.ydbio.2017.02.020",

language = "English",

volume = "424",

pages = "105--112",

journal = "Developmental Biology",

issn = "0012-1606",

publisher = "Elsevier Science Inc.",

number = "2",

}

RIS

TY - JOUR

T1 - Cellular aspects of gonadal atrophy in Drosophila P-M hybrid dysgenesis

AU - Dorogova, Natalia V.

AU - Bolobolova, Elena Us

AU - Zakharenko, Lyudmila P.

PY - 2017/4/15

Y1 - 2017/4/15

N2 - Gonadal atrophy is the most typical and dramatic manifestation of intraspecific hybrid dysgenesis syndrome leading to sterility in Drosophila melanogaster dysgenic progeny. The P-M system of hybrid dysgenesis is primarily associated with germ cell degeneration during the early stages of Drosophila embryonic development at elevated temperatures. In the present study, we have defined the phase of germ cell death as beginning at the end of embryogenesis immediately following gonad formation. However, the temperature-dependent screening of germ cell developmental patterns in the dysgenic background showed that early germ cells are susceptible to the hybrid dysgenesis at any Drosophila life-cycle stage, including in the imago. Electron microscopy of germ cells after dysgenesis induction revealed significant changes in subcellular structure, especially mitochondria, prior to cellular breakdown. The mitochondrial pathology can promote the activation of cell death pathways in dysgenic germ cells, which leads to gonadal atrophy.

AB - Gonadal atrophy is the most typical and dramatic manifestation of intraspecific hybrid dysgenesis syndrome leading to sterility in Drosophila melanogaster dysgenic progeny. The P-M system of hybrid dysgenesis is primarily associated with germ cell degeneration during the early stages of Drosophila embryonic development at elevated temperatures. In the present study, we have defined the phase of germ cell death as beginning at the end of embryogenesis immediately following gonad formation. However, the temperature-dependent screening of germ cell developmental patterns in the dysgenic background showed that early germ cells are susceptible to the hybrid dysgenesis at any Drosophila life-cycle stage, including in the imago. Electron microscopy of germ cells after dysgenesis induction revealed significant changes in subcellular structure, especially mitochondria, prior to cellular breakdown. The mitochondrial pathology can promote the activation of cell death pathways in dysgenic germ cells, which leads to gonadal atrophy.

KW - Cell death

KW - Drosophila

KW - Germ cell

KW - Hybrid dysgenesis

KW - Oogenesis

KW - Spermatogenesis

KW - Germ Cells/pathology

KW - Temperature

KW - Mitochondria/metabolism

KW - Male

KW - Atrophy

KW - Drosophila melanogaster/genetics

KW - Phenotype

KW - Animals

KW - Hybridization, Genetic

KW - Gonads/metabolism

KW - Female

KW - MITOCHONDRIA

KW - DEATH

KW - STERILITY

KW - FEMALE

KW - ELEMENTS

KW - MELANOGASTER

UR - http://www.scopus.com/inward/record.url?scp=85015012995&partnerID=8YFLogxK

U2 - 10.1016/j.ydbio.2017.02.020

DO - 10.1016/j.ydbio.2017.02.020

M3 - Article

C2 - 28283407

AN - SCOPUS:85015012995

VL - 424

SP - 105

EP - 112

JO - Developmental Biology

JF - Developmental Biology

SN - 0012-1606

IS - 2

ER -

ID: 10040856