CYCLIN-DEPENDENT KINASEs (CDKs) are the central gatekeepers of cell cycle progression and conserved in all eukaryotes. In this study, the Arabidopsis thaliana master cell cycle regulator CDKA;1 was functionally analyzed. CDKA;1 is a single gene in Arabidopsis and homologous to the human Cdk1 and the yeast cdc2/CDC28. Screening of two T-DNA insertion mutant collections resulted in the isolation of two independent cdka;1 null mutant alleles, which displayed the same phenotype. CDKA;1 was found to be required for both the sporophytic and the male gametophytic generations of the flowering plant Arabidopsis. While during sporophyte development, heterozygous mutant plants were unaffected, homozygous cdka;1 mutants were not viable and died as young embryos. During male gametophyte (pollen) development, the lack of CDKA;1 function caused a cell cycle arrest in the G2 phase prior to the last mitotic division. This cell cycle defect led to cdka;1 mutant pollen with only one instead of the usual two sperm cells. Nevertheless, the mutant cdka;1 pollen was viable and could fertilize the female gametophyte (embryo sac). Because cdka;1 pollen grains had only one instead of two sperm cells, they only performed single fertilization and thus, disrupted the double fertilization event characteristic of flowering plants. Interestingly, the cdka;1 mutant single fertilization exclusively targeted the egg cell, leaving the progenitor of the endosperm, the central cell, unfertilized. However, upon cdka;1 fertilization of the egg cell, not only the embryo started to develop, but the unfertilized central cell nucleus also began to divide. This onset of endosperm development without fertilization revealed a hitherto unrecognized endosperm proliferation signal emitted from the fertilization of the egg cell. The autonomous endosperm in cdka;1-fertilized seeds only underwent up to five nuclear division cycles before it stopped proliferating, followed by an early abortion of the whole seed. Thus, the cdka;1 mutant belongs to a rare class of paternal effect mutants that cause seed abortion irrespective of the genetic constitution of the female partner. In order to enhance endosperm proliferation in cdka;1-fertilized seeds, cdka;1 pollen was crossed to various fis-class mutants. These mutants are defective in the maternally inherited FIS-complex, a Polycomb-group repressive complex controlling genomic imprinting in the endosperm. In fis-class mutants, autonomous endosperm develops in the absence of fertilization. When fertilized, the fis-class mutant endosperm over-proliferates and due to a maternal effect these seeds abort later during development. The endosperm development in cdka;1-fertilized fis-mutant seeds was substantially enhanced and led to a partial rescue of the cdka;1-mediated seed abortion. Unexpectedly, the maternally conferred seed abortion caused by fis-class mutants was also partially reversed, producing viable seeds among the fis-class x cdka;1 offspring. This rescue was characterized by a down-regulated expression of the MADS-box transcription factor PHERES1, a downstream target of FIS-complex repression which is highly over-expressed in fertilized fis-class mutants. The down-regulation of PHERES1 in fis-class x cdka;1 endosperm suggests that the lack of paternal expression in combination with the defective gene repression of fis-class mutants results in a more balanced gene dosage of PHERES1 and potentially other genes of which the dosage is pivotal for regular seed development. These results indicate that the FIS-complex is not essential for endosperm development, but is important to harmonize maternal and paternal gene expression by the control of imprinting in the female genome. Furthermore, these data demonstrate that the paternal genome is not required for functional endosperm development if maternally derived genomic imprinting is bypassed due to mutations in the FIS-complex. The finding that a solely maternally derived endosperm can sustain seed development supports a hypothesis raised by Eduard Strasburger, who proposed in 1900 that the endosperm of flowering plants is of female gametophytic origin and that central cell fertilization might have evolved as a trigger to start endosperm proliferation