Similar Datasets
Project description:Historically, xenia effects were hypothesized to be unique genetic contributions of pollen to seed phenotype, but most examples represent standard complementation of Mendelian traits. We identified the imprinted dosage-effect defective1 (ded1) locus in maize (Zea mays) as a paternal regulator of seed size and development. Hypomorphic alleles show a 5-10% seed weight reduction when ded1 is transmitted through the male, while homozygous mutants are defective with a 70-90% seed weight reduction. Ded1 encodes an R2R3-MYB transcription factor expressed specifically during early endosperm development with paternal allele bias. DED1 directly activates early endosperm genes and endosperm adjacent to scutellum cell layer genes, while directly repressing late grain-fill genes. These results demonstrate xenia as originally defined: Imprinting of Ded1 causes the paternal allele to set the pace of endosperm development thereby influencing grain set and size.
| S-EPMC9470594 | biostudies-literature
Project description:Paternal imprinting of dosage-effect defective1 contributes to seed weight xenia in maize
| PRJNA759897 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-08-23 | GSE193307 | GEO
Project description:To elucidate the mechanisms underlying seed development in maize, comprehensive RNA-seq analyses were conducted on Zhengdan1002 (ZD1002), Zhengdan958 (ZD958), and their parental lines during seven seed developmental stages. We found that gene expression levels were largely nonadditive in hybrids and that cis-only or trans × cis pattern played a large role in hybrid gene regulation during seed developmental stage. Weighted gene co-expression network (WGCNA) analysis showed that 36 modules were highly correlated (r = -0.90-0.92, p < 0.05) with kernel weight, length, and width during seed development. Forty-five transcription factors and 38 ribosomal protein genes were identified as major hub genes determining seed size/weight. We also described a network hub, Auxin Response Factor 12 of maize (ZmARF12), a member of a family of transcription factor that mediate gene expression in response to auxin, potentially links auxin signal pathways, cell division, and the size of the seeds. The ZmARF12 mutant exhibited larger seed size and higher grain weight. ZmARF12 transcription was negatively associated with cell division during seed development, which was confirmed by evaluating the yield of protoplasts that isolated from the kernels of the mutant and other inbred lines. Transient knock-down of ZmARF12 in maize plants facilitated cell expansion and division, whereas transient silencing of its potential interactor ZmIAA8 impaired cell division. ZmIAA8 expression was repressed in the ZmARF12 over-expressed protoplasts. The mutant phenotype and the genetics studies presented here illustrated evidence that ZmARF12 is a cell division repressor, and potentially determines the final seed size.
| S-EPMC8882617 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2019-05-01 | GSE126932 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-08-31 | GSE172332 | GEO
Project description:In mammals, mothers are the primary caregiver, programmed, in part, by hormones produced during pregnancy. High-quality maternal care is essential for the survival and lifelong health of offspring. We previously showed that the paternally silenced imprinted gene pleckstrin homology-like domain family A member 2 (Phlda2) functions to negatively regulate a single lineage in the mouse placenta called the spongiotrophoblast, a major source of hormones in pregnancy. Consequently, the offspring's Phlda2 gene dosage may influence the quality of care provided by the mother. Here, we show that wild-type (WT) female mice exposed to offspring with three different doses of the maternally expressed Phlda2 gene-two active alleles, one active allele (the extant state), and loss of function-show changes in the maternal hypothalamus and hippocampus during pregnancy, regions important for maternal-care behaviour. After birth, WT dams exposed in utero to offspring with the highest Phlda2 dose exhibit decreased nursing and grooming of pups and increased focus on nest building. Conversely, 'paternalised' dams, exposed to the lowest Phlda2 dose, showed increased nurturing of their pups, increased self-directed behaviour, and a decreased focus on nest building, behaviour that was robustly maintained in the absence of genetically modified pups. This work raises the intriguing possibility that imprinting of Phlda2 contributed to increased maternal care during the evolution of mammals.
| S-EPMC6067684 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2011-07-12 | GSE29456 | GEO
Project description:In mammals and in plants, parental genome dosage imbalance deregulates embryo growth and might be involved in reproductive isolation between emerging new species. Increased dosage of maternal genomes represses growth while an increased dosage of paternal genomes has the opposite effect. These observations led to the discovery of imprinted genes, which are expressed by a single parental allele. It was further proposed in the frame of the parental conflict theory that parental genome imbalances are directly mirrored by antagonistic regulations of imprinted genes encoding maternal growth inhibitors and paternal growth enhancers. However these hypotheses were never tested directly. Here, we investigated the effect of parental genome imbalance on the expression of Arabidopsis imprinted genes FERTILIZATION INDEPENDENT SEED2 (FIS2) and FLOWERING WAGENINGEN (FWA) controlled by DNA methylation, and MEDEA (MEA) and PHERES1 (PHE1) controlled by histone methylation. Genome dosage imbalance deregulated the expression of FIS2 and PHE1 in an antagonistic manner. In addition increased dosage of inactive alleles caused a loss of imprinting of FIS2 and MEA. Although FIS2 controls histone methylation, which represses MEA and PHE1 expression, the changes of PHE1 and MEA expression could not be fully accounted for by the corresponding fluctuations of FIS2 expression. Our results show that parental genome dosage imbalance deregulates imprinting using mechanisms, which are independent from known regulators of imprinting. The complexity of the network of regulations between expressed and silenced alleles of imprinted genes activated in response to parental dosage imbalance does not support simple models derived from the parental conflict hypothesis.
| S-EPMC2841625 | biostudies-literature
Project description:The placental epigenome plays a critical role in regulating mammalian growth and development. Alterations to placental methylation, often observed at imprinted genes, can lead to adverse pregnancy complications such as intrauterine growth restriction and preterm birth. Similar associations have been observed in offspring derived from advanced paternal age fathers. As parental age at time of conception continues to rise, the impact of advanced paternal age on these reproductive outcomes is a growing concern, but limited information is available on the molecular mechanisms affected in utero. This longitudinal murine research study thus investigated the impact of paternal aging on genomic imprinting in viable F1 embryonic portions of the placentas derived from the same paternal males when they were young (4-6 months) and when they aged (11-15 months). The use of a controlled outbred mouse model enabled analysis of offspring throughout the natural lifetime of the same paternal males and excluded confounding factors like female age or infertility. Firstly, paternal age significantly impacted embryonic placental weight, fetal weight and length. Targeted bisulfite sequencing was utilized to examine imprinted methylation at the Kcnq1ot1 imprinting control region, with significant hypermethylation observed upon natural paternal aging. Quantitative real-time PCR assessed imprinted gene expression levels at various imprinting clusters, resulting in transcript level alterations attributable to advanced paternal age. In summary, our results demonstrate a paternal age effect with dysregulation at numerous imprinted loci, providing a mechanism for future adverse placental and offspring health conditions.
| S-EPMC7059926 | biostudies-literature