Abstract
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.
Highlights
In mammals and plants, mothers differentiate distinctive structures specialized in the transport of maternal nutrients to the embryo, the mammalian placenta and the plant seed endosperm [1]
Our results suggest that parental dosage imbalance disrupts imprinting through interactions between imprinted genes and other unidentified regulators
We propose that the unexpected silencing of the maternal alleles of FERTILIZATION INDEPENDENT SEED2 (FIS2) in endosperm produced by (2nmat64npat) crosses could originate from increased paternal dosage of a paternally expressed imprinted inhibitor of FIS2 or from the activity of yet unidentified cis-elements
Summary
Mothers differentiate distinctive structures specialized in the transport of maternal nutrients to the embryo, the mammalian placenta and the plant seed endosperm [1]. Unilateral maternal contribution of nutrients results in an imbalanced parental contribution to the offspring Such imbalance has been considered, in the frame of the kinship theory, as a potential cause for parental conflict of interest over allocation of resources to embryos [2,3]. The parental conflict hypothesis, derived from the kinship theory, proposes a competition over resource allocation to the embryo between imprinted genes encoding paternally expressed enhancers of embryo growth (PEGs) and maternally expressed inhibitors of embryo growth (MIGs) [11] This hypothesis further suggests that increased maternal genome dosage results in increased levels of MIGs transcripts causing reduced embryo growth. The transcription factor PHERES1 (PHE1) is a paternally expressed imprinted gene in Arabidopsis, which could play a role as a PEG
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