SeeDev-binary@ldeleger:SeeDev-binary-15708976-1 JSONTXT

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{"target":"https://pubannotation.org/docs/sourcedb/SeeDev-binary@ldeleger/sourceid/SeeDev-binary-15708976-1","sourcedb":"SeeDev-binary@ldeleger","sourceid":"SeeDev-binary-15708976-1","text":"Arabidopsis APETALA2 (AP2) encodes a member of the AP2/EREBP (ethylene responsive element binding protein) class of transcription factors and is involved\nin the specification of floral organ identity, establishment of floral meristem identity, suppression of floral meristem indeterminancy,\nand development of the ovule and seed coat. Here, we show that loss-of-function ap2 mutations cause an increase in seed mass relative to that of wild-type seeds. Analysis of an allelic series of ap2 mutations showed that increases in seed mass corresponded with the severity of defects in flower structure, indicating that\nAP2 activity directly influences seed mass. Experiments with male-sterile plants and deflowered wild-type plants showed that\nreduced fertility of ap2 mutant plants due to abnormal flower structure accounted for only part of the increase in seed mass caused by strong ap2 mutant alleles. Reciprocal cross experiments showed that AP2 acts maternally to control seed mass. The maternal effect of AP2 on seed mass involves the regulation of both embryo cell number and cell size. We show further that ap2 mutations cause changes in the ratio of hexose to sucrose during seed development, opening the possibility that AP2 may control seed mass through its effects on sugar metabolism. Together, these results identify a role for AP2 in controlling seed 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