Concurrent X chromosome inactivation and upregulation during non-human primate preimplantation development revealed by single-cell RNA-sequencing

Ana Luíza Cidral, J. (Joana) Carvalho Moreira de Mello, Joost Gribnau, Lygia V. Pereira*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

1 Citation (Scopus)

Abstract

In mammals, dosage compensation of X-linked gene expression between males and females is achieved by inactivation of a single X chromosome in females, while upregulation of the single active X in males and females leads to X:autosome dosage balance. Studies in human embryos revealed that random X chromosome inactivation starts at the preimplantation stage and is not complete by day 12 of development. Alternatively, others proposed that dosage compensation in human preimplantation embryos is achieved by dampening expression from the two X chromosomes in females. Here, we characterize X-linked dosage compensation in another primate, the marmoset (Callithrix jacchus). Analyzing scRNA-seq data from preimplantation embryos, we detected upregulation of XIST at the morula stage, where female embryos presented a significantly higher expression of XIST than males. Moreover, we show an increase of X-linked monoallelically expressed genes in female embryos between the morula and late blastocyst stages, indicative of XCI. Nevertheless, dosage compensation was not achieved by the late blastocyst stage. Finally, we show that X:autosome dosage compensation is achieved at the 8-cell stage, and demonstrate that X chromosome dampening in females does not take place in the marmoset. Our work contributes to the elucidation of primate X-linked dosage compensation.

Original languageEnglish
Article number9624
JournalScientific Reports
Volume11
Issue number1
DOIs
Publication statusPublished - 5 May 2021

Bibliographical note

Funding Information:
This work was supported by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP, fellowship 2018/14.856-8, ALC). J.C.M.M is supported by the Oncode Institute.

Publisher Copyright:
© 2021, The Author(s).

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