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N6-methyladenosine (m6A) maintains maternal RNA stability in oocytes. Here, the authors identify demethylase ALKBH5 as a key determinant of oocyte quality and unveil the facilitating role of ALKBH5-mediated m6A removal in maternal RNA decay.

Development of methods for simultaneous single cell analysis of transcription and translation is still underway. Here, Hu et al. develop single-cell transcriptome and translatome dual-omics on human oocytes, which enables them to identify OOSP2 as an induction factor during human oocyte maturation.

Interpolar microtubules were thought to be indispensable for eukaryotic cell division. Here, Akera and colleagues demonstrate that the second division of meiosis in yeast can occur in the absence of interpolar microtubules, and identify the forespore membrane as a force producing structure in cell division.

The authors developed a microfluidic device, FIND-Chip, designed to automate and enhance oocyte recovery from follicular fluid, a process traditionally done manually. When used in clinical settings, the device recovered additional oocytes missed during manual screening, substantially increasing the number of viable oocytes available for in vitro fertilization.

Oocyte meiosis must achieve spindle bipolarization without predefined spatial cues. Yoshida et al. demonstrate that spindle bipolarization during meiosis I in mouse oocytes requires kinetochores to prevent chromosome segregation errors, a phenomenon that does not occur in error-prone human oocytes.

The authors report a computational framework for determining the meiotic/mitotic origin of nondisjunction (NDJ) in trisomies without parental data. Applying this to Down syndrome, they uncover links between NDJ error stage and leukemia genomics.

IVF protocols are designed for the typical patient with infertility, but personalization can improve clinical outcomes. Here, authors show potential of AI methods to identify follicles that optimize clinical outcomes.

The oocyte environment is critical for its development. Conti and colleagues demonstrate that, in mouse, amphiregulin-stimulated somatic cumulus cells promote translation of maternal mRNAs in the oocyte in a manner dependent on oocyte PI(3)K signalling.

Xu et al. establish the importance of H2A.Z in mouse oocyte development. H2A.Z is incorporated into chromatin at promoters and putative enhancers, and its presence promotes histone acetylation in fully grown oocytes.

At puberty, hormones stimulate mammalian oocytes to resume meiosis, which is linked to dynamic epigenetic changes, but what controls such changes are unknown. Here, Kim et al. identify LSD1, a lysine demethylase, as regulating histone methylation at meiotic progression and also female fertility.

Gestational diabetes milletus (GDM) may have impairments on offspring health. Here, the authors suggest that the increase of EZH2 is an important reason for the disrupted DNA methylome in oocytes exposed to GDM, which may be associated with the transgenerational inheritance of the metabolic disorders.

Vanni et al. show a role for microtubules in YAP/TAZ mechanosignalling. Mechanoresponsive microtubule reorganization into centrosomal arrays allows for AMOT delivery to pericentrosomal proteasomes and degradation, leading to YAP/TAZ activation.

Wu et al. optimized the m⁶A mapping method for ultralow-input materials and characterized the transcriptome-wide landscape of m⁶A methylation in mouse oocytes and early embryos.

Pregestational hyperglycaemia in mothers increases the probability of glucose intolerance in the offspring, an effect controlled by TET3-dependent DNA demethylation of genes involved in insulin secretion.

mRNAs are known to be decorated with m5C at a low-to-medium level. Here, the authors generate atlases of mRNA m5C during animal development in 6 species and identify convergent and unexpected massive methylation of maternal mRNAs by NSUN2 and NSUN6.

Granulosa cells are the key lineage driving continuous folliculogenesis. Here, the authors reveal that the transcription factor Fosl2 reconfigures chromatin state in these cells and coordinates vital signalling pathways for ovulation and reproduction.

Alpha-synuclein (αSyn) aggregates implicated in synucleinopathies can be amplified by a seed amplification assay (SAA). Here, the authors show that SAA amplified αSyn aggregates from the CSF of a multiple system atrophy patient retain the biological and structural properties of the aggregates deposited in the brain

Chia et al. show that developmental arrest after human nuclear transfer is associated with genetic instability, including DNA damage, which occurs during DNA replication and is influenced by the developmental origin of the transferred nucleus.

The authors show that telomere length resetting in embryos, a key determinant of healthy aging, is established by mitochondrial function at conception.

Mouse induced pluripotent stem cells derived from differentiated fibroblasts could be converted from male (XY) to female (XX), resulting in cells that could form oocytes and give rise to offspring after fertilization.

Foreign body response can result in failure of biomaterials in vivo. Solvent-free crystals containing anti-fibrotic drugs now show the potential for long-term inhibition of fibrosis on a number of implantable devices in rodents and non-human primates.

Eight transcription factors are identified that, when overexpressed, are sufficient to grow oocyte-like cells from mouse pluripotent stem cells.

Oocyte meiotic defects increase with age and contribute to decreased oocyte quality. Here the authors show that granulosa cell mevalonate pathway abnormalities contribute to aneuploidy during ovarian aging and that supplementation with mevalonate metabolites improves oocyte quality, providing a potential therapeutic strategy for promoting female reproductive longevity.

Hundreds of genetic loci associated with age at menopause, combined with experimental evidence in mice, highlight mechanisms of reproductive ageing across the lifespan.

Mammalian oocyte maturation involves two asymmetric meiotic divisions that require the positioning of the meiotic spindle near the cortical area from which the extrusion of the polar bodies occurs. Li and colleagues show that the nucleating activity of the Arp2/3 complex, localized at the cortical actin cap, induces actin-filament flow away from the complex, creating a cytoplasmic streaming that pushes the spindle towards the cortex.

The authors develop a system to erase DNA methylation at H19-DMR in mouse sperm. Despite loss, methylation partly recovers via H3K9me3 after fertilization, revealing partial intergenerational epigenetic inheritance.

Low IVF efficiency is in part due to fertilization failure, though little is known about why retrieved oocytes vary in this regard. Here they show that oocyte maturation and nurse cell contacts are disrupted by superovulation and aging, and propose nurse cell markers to predict success of fertilized eggs.

The authors show that ELL3 maintains chromosomal ploidy by promoting spindle assembly and driving chromosome movement in oocytes. Deficiency of ELL3 results in oocyte aneuploidy and may lead to early miscarriage.

Mutations in mitochondrial DNA cause a wide range of disorders in humans, with a high prevalence; here it is shown that the nucleus of an affected woman’s egg could be inserted into healthy donor egg cytoplasm by spindle transfer, allowing the birth of healthy offspring.

Shao et al. report that FUS interacts with the transcriptional coactivator TAZ, maintaining liquid-like properties of TAZ biomolecular condensates and enhancing TAZ transcriptional activity.

As oocytes age the frequency of chromosome segregation errors during meiosis I increases. Here the authors use live imaging of oocytes from naturally aged mice to provide direct evidence that bivalent separation into univalents is the primary defect responsible for age-related aneuploidy.

Here the authors apply low-input methyl RNA immunoprecipitation and sequencing to map the N⁶-methyladenosine landscape during mouse oocyte and early embryo development. They show that RNAs derived from retrotransposons are often N⁶-methyladenosine marked and so are many genes important for the maternal-to-zygotic transition.

H2AK119ub1 and H3K27me3 have different genome-wide dynamics in mouse preimplantation embryos. Loss of H2AK119ub1, but not H3K27me3, causes premature activation of developmental genes during zygotic genome activation.