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    Home > Biochemistry News > Biotechnology News > An epigenetic cause of miscarriage found and cured

    An epigenetic cause of miscarriage found and cured

    • Last Update: 2022-05-13
    • Source: Internet
    • Author: User
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    A cartoon rendering of the first experiment
    .
    (Left) Normal condition of wild-type mice

    .
    (Middle) Maternal Xist is active and lethal to males when eggs do not contain H3K27 trimethylation

    .
    (Right) Additional knockout (KO) of Xist in pregnant mice prevents prenatal death (miscarriage) in male tilt

    .
    In addition, KO of other genes that failed to imprint rescued enlarged maternal placenta (not described)

    .

    Researchers led by Azusa Inoue at the Riken Center for Integrative Medical Sciences (IMS) have discovered a gene that causes prenatal death when egg cells lack key intergenerational instructions
    .
    The study, published April 28 in the journal Genes & Development, shows that in mice, failure of epigenetic suppression of an X-chromosome gene called Xist leads to miscarriage and development exception

    .

    Inoue said: "This study identifies genes critical to fetal development whose expression is controlled by histone modifications that are passed on from the egg to the next generation
    .
    These findings have implications for understanding infertility and developing treatments.
    meaning

    .
    "

    For the embryo to develop properly, the egg and sperm need to receive important biological instructions before they meet
    .
    Once an egg is fertilized, some of these instructions tell genes to turn on or off depending on whether they came from the mother or the father

    .
    This process, known as genomic imprinting, is the focus of the new study

    .

    When modifications in gene expression are passed on to the next generation, they are called trans-representative epigenetic changes because they are heritable changes even when the DNA code remains the same
    .
    Inoue and his team have been studying a specific set of trans-representative epigenetic instructions known as histone H3 lysine 27 (H3K27) trimethylation

    .
    In previous research, they found that blocking these instructions led to prenatal death, especially in male embryos, and also to an enlarged placenta in the mother

    .
    The new study asked whether these results were directly related to the imprint of failure

    .

    The study began by knocking out a gene required for H3K27 trimethylation in eggs so that it could not be passed on from generation to generation
    .
    Next, the team added the knocked-out Xist gene to the eggs

    .
    Since male offspring tend to die, the researchers suspect a gene on the sex chromosome is the culprit

    .
    It turns out that nine maternal genes are known to be suppressed in embryos, while those from the paternal line are suppressed

    .
    Only one, Xist, is on the X chromosome

    .

    The result is almost as expected
    .
    Prenatal mortality was greatly reduced, and male-tilted mortality disappeared after Xist was knocked out

    .
    This suggests that Xist imprint failure is the cause of prenatal death

    .
    However, the placenta is still enlarged

    .
    Since this could be related to the overexpression of eight other genes that failed to imprint, the team created eight different deletion mutants in double knockout embryos

    .
    They found placentas of normal size for three of the genes

    .

    "We were successful in curing a developmental defect in a mouse model that would otherwise suffer from prenatal death and placental malformations due to the lack of trans-representative epigenetic instructions from the mother," Inoue said
    .
    The researchers plan to conduct additional experiments.
    , to determine how these specific biological instructions are established when egg cells are produced, and whether environmental factors influence this process

    .

    Noncanonical imprinting sustains embryonic development and restrains placental overgrowth .
    Genes Dev.
    doi: 10.
    1101/gad.
    349390.
    122

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