Maternal messages to live by: a personal historical perspective

King, Mary Lou

doi:10.1002/dvg.23007

Cited by 3 publications

(3 citation statements)

References 102 publications

(106 reference statements)

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“…These results reveal a previously unrecognized function of ZAR1/2 in mammalian oocytes and indicate that the previously described role of ZAR1/2 in ZGA is secondary to oocyte maturation defects. The stringent definition of a maternal factor is ‘a protein supplied by the mother but solely functioning in the progeny’ (54,55); therefore, a true maternal effect gene determines the phenotype of the offspring but not the mother itself. In this sense, Zar1 , known for decades as a representative mammalian maternal effect gene, is actually not a true maternal effect gene.…”

Section: Discussionmentioning

confidence: 99%

ZAR1 and ZAR2 are required for oocyte meiotic maturation by regulating the maternal transcriptome and mRNA translational activation

Yan

Zhu

et al. 2019

Nucleic Acids Research

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Zar1 was one of the earliest mammalian maternal-effect genes to be identified. Embryos derived from Zar1-null female mice are blocked before zygotic genome activation; however, the underlying mechanism remains unclear. By knocking out Zar1 and its homolog Zar2 in mice, we revealed a novel function of these genes in oocyte meiotic maturation. Zar1/2-deleted oocytes displayed delayed meiotic resumption and polar body-1 emission and a higher incidence of abnormal meiotic spindle formation and chromosome aneuploidy. The grown oocytes of Zar1/2-null mice contained decreased levels of many maternal mRNAs and displayed a reduced level of protein synthesis. Key maturation-associated changes failed to occur in the Zar1/2-null oocytes, including the translational activation of maternal mRNAs encoding the cell-cycle proteins cyclin B1 and WEE2, as well as maternal-to-zygotic transition (MZT) licensing factor BTG4. Consequently, maternal mRNA decay was impaired and MZT was abolished. ZAR1/2 bound mRNAs to regulate the translational activity of their 3′-UTRs and interacted with other oocyte proteins, including mRNA-stabilizing protein MSY2 and cytoplasmic lattice components. These results countered the traditional view that ZAR1 only functions after fertilization and highlight a previously unrecognized role of ZAR1/2 in regulating the maternal transcriptome and translational activation in maturing oocytes.

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Section: Discussionmentioning

confidence: 99%

ZAR1 and ZAR2 are required for oocyte meiotic maturation by regulating the maternal transcriptome and mRNA translational activation

Yan

Zhu

et al. 2019

Nucleic Acids Research

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“…In non-mammalian species, the importance of MEGs in early development is well documented. 5 , 6 , 7 , 8 In contrast, relatively little is known about the role of MEGs in mammalian development. However, the first mammalian MEGs were reported in 2000, 9 and the number of such genes has subsequently increased steadily.…”

Section: Introductionmentioning

confidence: 99%

Maternal effect genes: Update and review of evidence for a link with birth defects

Mitchell

2022

Human Genetics and Genomics Advances

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Summary Maternal effect genes (MEGs) encode factors (e.g., RNA) that are present in the oocyte and required for early embryonic development. Hence, while these genes and gene products are of maternal origin, their phenotypic consequences result from effects on the embryo. The first mammalian MEGs were identified in the mouse in 2000 and were associated with early embryonic loss in the offspring of homozygous null females. In humans, the first MEG was identified in 2006, in women who had experienced a range of adverse reproductive outcomes, including hydatidiform moles, spontaneous abortions, and stillbirths. Over 80 mammalian MEGs have subsequently been identified, including several that have been associated with phenotypes in humans. In general, pathogenic variants in MEGs or the absence of MEG products are associated with a spectrum of adverse outcomes, which in humans range from zygotic cleavage failure to offspring with multi-locus imprinting disorders. Although less established, there is also evidence that MEGs are associated with structural birth defects (e.g., craniofacial malformations, congenital heart defects). This review provides an updated summary of mammalian MEGs reported in the literature through early 2021, as well as an overview of the evidence for a link between MEGs and structural birth defects.

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“…The importance of MEGs in the development of non-mammalian species has been established. 2 , 3 , 4 , 5 Although less is known about the role of MEGs in the development of mammals, the first mammalian MEG was reported in 2000, 6 and over 80 mammalian MEGs have subsequently been identified. 7 Most evidence implicating these genes as MEGs comes from animal studies.…”

Section: Introductionmentioning

confidence: 99%