Correct timing of developmental phase transitions is critical for the survival and fitness of plants. Developmental phase transitions in plants are partially promoted by controlling relevant genes into active or repressive status. Polycomb Repressive Complex1 (PRC1) and PRC2, originally identified in Drosophila, are essential in initiating and/or maintaining genes in repressive status to mediate developmental phase transitions. Our review summarizes mechanisms in which the embryo-to-seedling transition, the juvenile-to-adult transition, and vegetative-to-reproductive transition in plants are mediated by PRC1 and PRC2, and suggests that PRC1 could act either before or after PRC2, or that they could function independently of each other. Details of the exact components of PRC1 and PRC2 in each developmental phase transitions and how they are recruited or removed will need to be addressed in the future.

The juvenile-to-adult vegetative phase change in flowering plants is mediated by a decrease in miR156 levels. Downregulation of MIR156A/MIR156C, the two major sources of miR156, is accompanied by a decrease in acetylation of histone 3 lysine 27 (H3K27ac) and an increase in trimethylation of H3K27 (H3K27me3) at MIR156A/MIR156C in Arabidopsis.Here, we show that histone deacetylase 9 (HDA9) is recruited to MIR156A/MIR156C during the juvenile phase and associates with the CHD3 chromatin remodeler PICKLE (PKL) to erase H3K27ac at MIR156A/MIR156C.H2Aub and H3K27me3 become enriched at MIR156A/MIR156C, and the recruitment of Polycomb Repressive Complex 2 (PRC2) to MIR156A/MIR156C is partially dependent on the activities of PKL and HDA9.Our results suggest that PKL associates with histone deacetylases to erase H3K27ac and promote PRC1 and PRC2 activities to mediate vegetative phase change and maintain plants in the adult phase after the phase transition.

Flagellar motility is essential for the cell morphology, viability, and virulence of pathogenic kinetoplastids. Trypanosoma brucei flagella beat with a bending wave that propagates from the flagellum’s tip to its base, rather than base-to-tip as in other eukaryotes. Thousands of dynein motor proteins coordinate their activity to drive ciliary bending wave propagation. Dynein-associated light and intermediate chains regulate the biophysical mechanisms of axonemal dynein. Tctex-type outer arm dynein light chain 2 (LC2) regulates flagellar bending wave propagation direction, amplitude, and frequency in Chlamydomonas reinhardtii. However, the role of Tctex-type light chains in regulating T. brucei motility is unknown. Here, we used a combination of bioinformatics, in-situ molecular tagging, and immunofluorescence microscopy to identify a Tctex-type light chain in the procyclic form of T. brucei (TbLC2). We knocked down TbLC2 expression using RNAi in both wild-type and FLAM3, a flagellar attachment zone protein, knockdown cells and quantified TbLC2’s effects on trypanosome cell biology and biophysics. We found that TbLC2 knockdown reduced the directional persistence of trypanosome cell swimming, induced an asymmetric ciliary bending waveform, modulated the bias between the base-to-tip and tip-to-base beating modes, and increased the beating frequency. Together, our findings are consistent with a model of TbLC2 as a down-regulator of axonemal dynein activity that stabilizes the forward tip-to-base beating ciliary waveform characteristic of trypanosome cells. Our work sheds light on axonemal dynein regulation mechanisms that contribute to pathogenic kinetoplastids’ unique tip-to-base ciliary beating nature and how those mechanisms underlie dynein-driven ciliary motility more generally.

converted into complex waveforms. The conversion mechanism has remained a long-standing unresolved issue. Since Chlamydomonas flagella change their waveforms from a flagellar type to a ciliary type, responding to the increase in intracellular Ca 2þ concentrations, this response may provide a hint for the mechanism of the flagellar waveform generation. To provides the spatial arrangement of axonemal components on doublet microtubules of Chlamydomonas under different Ca 2þ concentrations and the change in the helical arrangement of these components, we carried out the small-angle X-ray fiber diffraction. The axonemes were oriented in a physiological solution by continuous shear-flow and were exposed to intense and stable X-rays in the synchrotron radiation facility SPring-8 BL40XU. The diffraction patterns showed the layer lines of the radial-spokeoriginating 48-nm and dynein-arm originating 24-nm reflections at the low Ca 2þ concentrations while they decreased their intensities in the high Ca 2þ concentrations, suggesting the change in the helical symmetry of the doublets of the axoneme. The relation between the helical symmetry and the flagella waveform change was examined by a numerical model. In this model, the change of the helical symmetry was incorporated as a positional shift of the antagonistic motor pairs. The simulation showed that the amplitude/frequency of the flagellar beating varies with the shift of the motors. It was also found that the effect of the shift increases the asymmetry of the flagellar beat when the axonemal structure was considered to be asymmetric. This work was supported by JSPS KAKENHI(26440089, 17K07376, JP16H06280, the Takeda Science Foundation (K.O).

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