Biology subjects

Kajita, S.

Publications and source records attributed to Kajita, S..

3 recordsLinked to original sources

bioRxiv2026

Identifying and engineering the molecular origins of lignin color for predictive staining of plant tissues.

Lignins in plant biomass are carbon-negative aromatic biopolymers which hold tremendous potential as multipurpose resources for sustainable bioeconomy, limited only by their chemical heterogeneity. Plant lignified tissues, such as sapwood and seed coats, vary in colors within and between species, indicating that specific lignin topochemistries determine the different colors. Yet, the responsible lignin chromogen(s) are unknown. We developed chemical imaging using UV-Vis microspectroscopy to link lignin color to topochemistry in isolates and plant samples. Using synthetic and technical lignins, we identified the different stable chromogens as homomeric lignin substructures varying in size, unit chemistry and interunit linkages. We controlled the accumulation of specific lignin chromogens using genetic engineering to similarly stain lignified tissues from different plant species. We established plant tissue engineering to cast plant tissues with pre-determined color by adjusting lignin topochemistries. We proved that biotechnological manipulation of the identified lignin chromogens predictably and stably stains lignified plant tissues.

bioengineering↗

bioRxiv2021

Specific and dynamic lignification at the cell-type level controls plant physiology and adaptability

The biopolymer lignin, deposited in the cell walls of vascular cells, is essential for long-distance water conduction and structural support of plants. Independently of the species, each different vascular cell type contains a conserved lignin chemistry with specific aromatic and aliphatic substitutions. Yet, the biological role of this conserved and specific lignin chemistry for each cell type remained unclear. Herein, we investigate the role of specific lignin chemistries for cellular function by producing single cell analyses on vascular cell morphotypes, all enabling sap conduction but differing in morphology. We found that specific lignin chemistries accumulate in each morphotype. Moreover, lignin accumulates dynamically, increasing in quantity and changing composition, to alter the cell wall biomechanics of each morphotype during their maturation. For similar aromatic substitution, residues with alcohol aliphatic functions increased stiffness whereas aldehydes increased flexibility. Modifying this specific lignin chemistry impairs the cell wall biomechanics of each morphotype and consequently reduces their capacity to optimally conduct water in normal conditions, and to recover from drought. Altogether, lignin chemistry is differently controlled for each sap conducting cell types during their maturation to dynamically adjust their biomechanics and hydraulic properties to adapt to developmental and environmental constraints.

plant biology↗

bioRxiv2019

A novel nuclear speckle factor, USP42, promotes homologous recombination repair by resolving DNA double-strand break induced R-loop

The nucleus of mammalian cells is highly compartmentalized by nuclear bodies, including nuclear speckles. While nuclear bodies are known to function in regulating gene expression, their involvement in DNA repair has not been actively investigated. Here, our focused screen for nuclear speckle factors involved in homologous recombination (HR), which is a faithful DNA double-strand break (DSB) repair mechanism, revealed that nuclear speckle factors regulating transcription are potentially involved in the regulation of HR. Among the top hits, we provide evidence showing that USP42, which is a deubiquitylating enzyme and a hitherto unidentified nuclear speckles factor, promotes HR by facilitating BRCA1 recruitment to DSB sites and DNA-end resection. We further showed that USP42 localizes to nuclear speckles via an intrinsically disordered region, which is required for efficient HR. Furthermore, we established that USP42 interacts with DHX9, which possesses DNA-RNA helicase activity, and is required for efficient resolution of DSB-induced R-loop. Mechanistically, USP42 antagonizes mono-ubiquitylation of DHX9 that is evoked after DSB induction. In conclusion, our data propose a model in which a novel nuclear speckle factor, USP42, facilitates DSB-induced R-loop resolution, BRCA1 loading to DSB sites and preferential DSB repair by HR, indicating the importance of spatial regulation of DSB repair choice mediated by nuclear bodies.\n\nSignificant statementDefects in the repair of DNA double-strand break (DSB), which is one of the most harmful DNA insults, cause human diseases including cancers. It has been suggested that DSBs generated in the coding region tend to be repaired by homologous recombination (HR) that is error-free DSB repair pathway. To reveal the spatial regulation of HR, in this study, we investigated the potential contribution of nuclear bodies, especially nuclear speckles, to HR, identifying a deubiquitylating enzyme USP42 as a HR promoting factor. We found that USP42 deubiquitylates DHX9, facilitates resolution of DNA-RNA hybrid structure and enhances HR through BRCA1 loading to DSB sites.\n\nClassificationBiological Sciences, Cell Biology

cell biology↗