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Mitofusin 1 is required for oocyte growth and communication with follicular somatic cells
Author(s) -
Carvalho Karen F.,
Machado Thiago S.,
Garcia Bruna M.,
Zangirolamo Amanda F.,
Macabelli Carolina H.,
Sugiyama Fabrícia H. C.,
Grejo Mateus P.,
Augusto Neto J. Djaci,
Tostes Katiane,
Ribeiro Fernanda K. S.,
Sarapião Fabiana D.,
Pandey Anand K.,
Nociti Ricardo P.,
Tizioto Polyana,
Coutinho Luiz Lehman,
Meirelles Flávio V.,
Guimarães Francisco E. G.,
Pernas Lena,
Seneda Marcelo M.,
Chiaratti Marcos R.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.201901761r
Subject(s) - mfn1 , mfn2 , oocyte , mitochondrial fusion , microbiology and biotechnology , biology , somatic cell , oocyte activation , folliculogenesis , genetics , mitochondrial dna , embryogenesis , embryo , gene
Abstract Mitochondrial function, largely regulated by the dynamics of this organelle, is inextricably linked to the oocyte health. In comparison with most somatic cells, mitochondria in oocytes are smaller and rounder in appearance, suggesting limited fusion. The functional implications of this distinct morphology, and how changes in the mitochondrial shape translate to mitochondrial function in oogenesis is little understood. We, therefore, asked whether the pro‐fusion proteins mitofusins 1 (MFN1) and 2 (MFN2) are required for the oocyte development. Here we show that oocyte‐specific deletion of Mfn1 , but not Mfn2 , prevents the oocyte growth and ovulation due to a block in folliculogenesis. We pinpoint the loss of oocyte growth and ovulation to impaired PI3K‐Akt signaling and disrupted oocyte‐somatic cell communication. In support, the double loss of Mfn1 and Mfn2 partially rescues the impaired PI3K‐Akt signaling and defects in oocyte development secondary to the single loss of Mfn1 . Together, this work demonstrates that the mitochondrial function influences the cellular signaling during the oocyte development, and highlights the importance of distinct, nonredundant roles of MFN1 and MFN2 in oogenesis.