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RESEARCH ARTICLE
Genetic and structural analysis of the in vivo functional redundancy between murine NANOS2 and NANOS3
Danelle Wright, Makoto Kiso, Yumiko Saga
Development 2021 148: dev191916 doi: 10.1242/dev.191916 Published 11 January 2021
Danelle Wright
1Department of Genetics, The Graduate University for Advanced Studies, SOKENDAI, Mishima 411-8540, Japan
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  • ORCID record for Danelle Wright
Makoto Kiso
2Department of Gene Function and Phenomics, Mammalian Development Laboratory, National Institute of Genetics, Mishima 411-8540, Japan
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Yumiko Saga
1Department of Genetics, The Graduate University for Advanced Studies, SOKENDAI, Mishima 411-8540, Japan
2Department of Gene Function and Phenomics, Mammalian Development Laboratory, National Institute of Genetics, Mishima 411-8540, Japan
3Department of Biological Sciences, Graduate School of Science, The University of Tokyo, Tokyo 113-0033, Japan
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  • For correspondence: ysaga@nig.ac.jp

Handling Editor: Haruhiko Koseki

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ABSTRACT

NANOS2 and NANOS3 are evolutionarily conserved RNA-binding proteins involved in murine germ cell development. NANOS3 is required for protection from apoptosis during migration and gonadal colonization in both sexes, whereas NANOS2 is male-specific and required for the male-type differentiation of germ cells. Ectopic NANOS2 rescues the functions of NANOS3, but NANOS3 cannot rescue NANOS2 function, even though its expression is upregulated in Nanos2-null conditions. It is unknown why NANOS3 cannot rescue NANOS2 function and it is unclear whether NANOS3 plays any role in male germ cell differentiation. To address these questions, we made conditional Nanos3/Nanos2 knockout mice and chimeric mice expressing chimeric NANOS proteins. Conditional double knockout of Nanos2 and Nanos3 led to the rapid loss of germ cells, and in vivo and in vitro experiments revealed that DND1 and NANOS2 binding is dependent on the specific NANOS2 zinc-finger structure. Moreover, murine NANOS3 failed to bind CNOT1, an interactor of NANOS2 at its N-terminal. Collectively, our study suggests that the inability of NANOS3 to rescue NANOS2 function is due to poor DND1 recruitment and CNOT1 binding.

Footnotes

  • Competing interests

    The authors declare no competing or financial interests.

  • Author contributions

    Conceptualization: D.W., Y.S.; Methodology: D.W., M.K., Y.S.; Validation: D.W.; Formal analysis: D.W.; Investigation: D.W.; Resources: M.K., Y.S.; Writing - original draft: D.W., Y.S.; Writing - review & editing: D.W., Y.S.; Visualization: D.W., Y.S.; Supervision: Y.S.; Project administration: Y.S.; Funding acquisition: Y.S.

  • Funding

    This work was supported by the Japan Society for the Promotion of Science KAKENHI grant numbers 16H06279 and 17H06166.

  • Data availability

    Single-cell RNA-seq data have been deposited into the DNA Data Bank of Japan (DDBJ) under accession number DRA011172.

  • Supplementary information

    Supplementary information available online at https://dev.biologists.org/lookup/doi/10.1242/dev.191916.supplemental

  • Received April 22, 2020.
  • Accepted November 4, 2020.
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Keywords

  • Germ cells
  • Mouse
  • Nanos
  • RNA-binding protein

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RESEARCH ARTICLE
Genetic and structural analysis of the in vivo functional redundancy between murine NANOS2 and NANOS3
Danelle Wright, Makoto Kiso, Yumiko Saga
Development 2021 148: dev191916 doi: 10.1242/dev.191916 Published 11 January 2021
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RESEARCH ARTICLE
Genetic and structural analysis of the in vivo functional redundancy between murine NANOS2 and NANOS3
Danelle Wright, Makoto Kiso, Yumiko Saga
Development 2021 148: dev191916 doi: 10.1242/dev.191916 Published 11 January 2021

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