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posted by Fnord666 on Monday July 13 2020, @05:18AM   Printer-friendly
from the right-sized-placentas dept.

Arthur T Knackerbracket has found the following story:

One reason a technique for cloning animals often results in oversized placentas, and hence failed births, has been uncovered in mice by an all-RIKEN team. This finding will help improve the success rate of the cloning method and could also shed light on fertility treatments for people.

[...] Now, Kimiko Inoue, Atsuo Ogura, and their co-workers, all at the RIKEN BioResource Research Center, have discovered that the overexpression of the largest imprinted microRNA clusters in mice is one of the main reasons why SCNT often produces placentas that are too large. When they corrected for this, they were able to double the birth rate.

A process known as genomic imprinting guides the early development of mammals by switching certain genes on and off as the embryo and placenta develop and grow. This can lead to the expression of genes from only one parent, depending on small molecules attached to the genetic sequence called epigenetic marks. The team found that SCNT placentas' lack of genomic imprinting based on the epigenetic mark histone methylation goes a long way to explaining their abnormal size.

[...] Inoue wasn't expecting to find that the culprit was a microRNA that didn't code for proteins. "I was surprised to discover that a non-protein-coding microRNA, and not a protein-coding gene, was the main cause of the oversized placentas produced by SCNT," she says.

The study has repercussions beyond SCNT. "We've demonstrated that non-coding microRNA plays an essential role in the healthy development of placentas," says Inoue. "I anticipate this will help us understand placental abnormalities and develop gene markers for assisted reproductive technologies for people."

-- submitted from IRC

Journal Reference:
Kimiko Inoue, Narumi Ogonuki, Satoshi Kamimura, et al. Loss of H3K27me3 imprinting in the Sfmbt2 miRNA cluster causes enlargement of cloned mouse placentas [open], Nature Communications (DOI: 10.1038/s41467-020-16044-8)


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  • (Score: 0) by Anonymous Coward on Monday July 13 2020, @04:51PM (2 children)

    by Anonymous Coward on Monday July 13 2020, @04:51PM (#1020442)

    While gestating, mother and embryo are in genetic conflict; embryo's genes' chances increase by more resources directed to that embryo, siblings' and mother's health notwithstanding, while mother's genes' chances increase by her producing more living offspring in total, i.e. larger litters and more pregnancies in a lifetime. The imprinting is part of ever-going tug-of-war between the two. Egg-laying and roe-spawning animals do not have imprinting.
    https://en.wikipedia.org/wiki/Genomic_imprinting#Imprinted_genes_in_other_animals [wikipedia.org]
    Naturally, if no maternal imprint is there, the embryo's genes, having evolved to work against its influence, totally overdo their thing.

  • (Score: 0) by Anonymous Coward on Monday July 13 2020, @05:05PM

    by Anonymous Coward on Monday July 13 2020, @05:05PM (#1020463)

    That will be fixed in version 3.0.

  • (Score: 0) by Anonymous Coward on Tuesday July 14 2020, @01:38PM

    by Anonymous Coward on Tuesday July 14 2020, @01:38PM (#1021218)

    So much of biology is co-op competitive.

    For instance, the two sexes need to work together to breed, but each competes against the other to put more of the burden on them. The results can be pretty extreme, on the one side, there are harem species, on the other is monogamy (or in the extreme case, reverse harems*).

    * https://en.wikipedia.org/wiki/African_jacana [wikipedia.org]