The MADS domain transcription factor AGAMOUS (AG) regulates floral meristem termination by preventing maintenance of the histone modification H3K27me3 along the KNUCKLES (KNU) coding sequence. At two days after AG binding, cell division has diluted the repressive mark H3K27me3, allowing activation of KNU transcription prior to floral meristem termination. However, how many other downstream genes are temporally regulated by this intrinsic epigenetic timer and what their functions are remain unknown. Here, we identify direct AG targets regulated through cell cycle–coupled H3K27me3 dilution in Arabidopsis thaliana. Expression of the targets KNU, AT HOOK MOTIF NUCLEAR LOCALIZED PROTEIN18 (AHL18), and PLATZ10 occurred later in plants with longer H3K27me3-marked regions. We established a mathematical model to predict timing of gene expression and manipulated temporal gene expression using the H3K27me3-marked del region from the KNU coding sequence. Increasing the number of del copies delayed and reduced KNU expression in a Polycomb Repressive Complex 2– and cell cycle–dependent manner. Furthermore, AHL18 was specifically expressed in stamens and caused developmental defects when mis-expressed. Finally, AHL18 bound to genes important for stamen growth. Our results suggest that AG controls the timing of expression of various target genes via cell cycle–coupled dilution of H3K27me3 for proper floral meristem termination and stamen development.
The termination of floral meristems is regulated by the MADS domain transcription factor AGAMOUS (AG) by passively diluting the H3K27me3 mark along the KNUCKLES (KNU) coding sequence. How many other downstream genes are similarly regulated by this intrinsic epigenetic timer and whether it can be harnessed for engineering synthetic circuits are unknown. Here, we describe a biotimer gene regulatory network downstream of AG and manipulate the timing of KNU expression through a synthetic system. We manipulated temporal gene expression using the del region from the KNU coding sequence, which is decorated by H3K27me3-marked nucleosomes. Increasing the number of del copies delayed and reduced KNU expression in a PRC2- and cell cycle-dependent manner. We propose that PRC2 deposits H3K27me3, while cell divisions dilute H3K27me3 accumulation on the extended KNU coding sequence. Our results shed light on temporal transitions governing flower development and provide a novel tool for tunable gene expression.
Locomotive syndrome (LS) is a condition in which a person's mobility is impaired due to musculoskeletal disorders caused by aging or lack of exercise, signaling an imminent need for primary nursing care. This study aims to develop a smartphone application that can distinguish the LS stage in a safe, simple, and quantifiable manner. Using a six-axes accelerometer built into the smartphone, acceleration and angular velocity data were collected from elderly subjects performing alternating one-legged stances at intervals of 2.66 s. Frequency analysis was then performed with a fast Fourier transform (FFT) and an autocorrelation coefficient to compare the data characteristics of subjects with and without LS. Due to huge individual variances, significant differences were not observed between LS and non-LS, and discriminating the LS stage using frequency analysis was considered difficult in the present study. In contrast, the autocorrelation coefficient showed significant differences between LS and non-LS in acceleration and angular velocity in specific directions. Using the autocorrelation coefficient of acceleration and angular velocity data to detect the presence of LS was concluded to be effective.
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