Abstract
The genetic network controlling flowering and flower development consists of a set of floral integrator genes that play a role in light sensing, hormone signaling and developmental pathways. These integrators activate the expression of meristem identity genes LEAFY (LFY) and APETALA1 (AP1) to initiate the flowering transition. However, how the expression of key genes, such as AP1, responds to diverse signals during flower development remains largely unknown. Here, we report that an Arabidopsis abnormal flower development inbred line (AFDL) exhibits a phenotype similar to the ap1 mutant, with delayed flowering time and a high frequency of transition of flower meristems into inflorescence meristems after flowering. The flower organs with an abnormal first whorl lack the second whorl and the increased number of inflorescences at the first- and second-whorl positions most closely resembled the phenotypes of ap1/cal double mutants. Interestingly, both normal and abnormal flowers coexisted in a single individual. Microarray and quantitative real-time PCR analysis revealed that the expression of AP1 was significantly reduced, while the expression of its interacting genes TERMINAL FLOWER 1 (TFL1), SHORT VEGETATIVE PHASE (SVP), AGAMOUS-like 24 (AGL24), SEPALLATA (SEP) and CAULIFLOWER (CAL) and upstream genes FLOWERING LOCUS C (FLC) and FLM were increased in AFDL, which could serve to explain its phenotype. The expression of genes responsive to different stimuli dramatically changed in AFDL relative to the wild type, as revealed by the differential display of transcripts, indicating that this expression variation is subject to a threshold, leading to an on/off expression pattern of the master regulatory gene (such as AP1) of flower development.
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Qi, X., Jiang, Y., Tang, F. et al. An Arabidopsis thaliana (Ler) inbred line AFDL exhibiting abnormal flower development mainly caused by reduced AP1 expression. Chin. Sci. Bull. 56, 39–47 (2011). https://doi.org/10.1007/s11434-010-4263-4
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DOI: https://doi.org/10.1007/s11434-010-4263-4