Biology subjects

Takagi, K.

Publications and source records attributed to Takagi, K..

6 recordsLinked to original sources

bioRxiv2026

Disruption of the single-copy GOLDEN2-like gene underlies the classical yellow and yellow-mutable mutations of Japanese morning glory

GOLDEN2-like (GLK) transcription factors are key regulators of chloroplast differentiation and photosynthetic gene expression. The classical yellow mutation in Japanese morning glory (Ipomoea nil) produces yellowish-green leaves, whereas an unstable allele, yellow-mutable, produces green somatic sectors on a yellowish-green background. The gene responsible for these mutations was identified as InGLK, which encodes a GOLDEN2-like transcription factor. The stable yellow mutant carried a 4-bp frameshift insertion in InGLK, whereas two yellow-mutable lines carried the Tpn1-family transposon Tpn12 in intron 5. Excision of Tpn12 in germinal revertants left short footprints and restored the green leaf phenotype. Genome searches identified InGLK as the sole GLK gene in I. nil. Pigment analysis of green somatic reversion sectors and yellowish-green background areas showed that most of the measured photosynthetic pigments were significantly reduced in the yellowish-green background, whereas the chlorophyll a/b ratio was unchanged. Chloroplasts in the yellowish-green tissue retained thylakoid-like membranes and starch granule-like structures but had less distinct grana-like stacks and sparse stromal lamellae-like structures. Wild-type-like chloroplast ultrastructure was restored in germinal revertants. These findings show that loss of function of a single-copy GLK gene broadly reduces photosynthetic pigment accumulation and alters chloroplast internal membrane organization. The yellow mutants of I. nil therefore provide a genetic system for examining non-redundant GLK function.

plant biology↗

bioRxiv2025

A lipid-driven, microbe-independent mechanism of acne via Lrig1+ follicular progenitor cells

Long-chain saturated fatty acids (lcSFAs) are abundant in the skin, but their pathogenic roles in acne remain unclear. In human sebum profiling, C16:0, the most abundant lcSFA, was the only fatty acid significantly elevated in acne and correlated with inflammatory comedone counts. We then established a mouse model that faithfully recapitulates human acne phenotypes, in which topical C16:0 penetrated the epidermis and induced sebocyte hyperplasia, comedogenesis, and follicular inflammation. Mechanistically, C16:0 activated keratinization and inflammatory pathways and drove sebocyte-lineage differentiation from Lrig1+progenitor cells, which function as cutaneous lipid sensors. These effects persisted in germ-free mice and were unaffected by fatty acid transporter modulation, while MyD88 signaling was partially required for inflammatory cell recruitment. Together, our findings identified C16:0 as a human acne-associated lipid that recapitulates disease hallmarks through a microbe-independent, lipid-driven pathway, highlighting Lrig1+cells as central hubs in remodeling of the pilosebaceous unit.

cell biology↗

bioRxiv2025

Postnatal interaction of size and shape in the human endocranium and brain structures

The uniqueness of human brain growth and development has been considered promising to understand the advanced cognitive ability of humans. Compared with that of chimpanzees, the human endocranium undergoes several characteristic shape changes immediately after birth, which has been termed "endocranial globularization." However, how the brain structures and surrounding neurocranium interact with each other during early development in the context of brain-neurocranium integration remains to be investigated. We observed shape changes in the human brain and endocranium during postnatal development using magnetic resonance imaging, and analyzed spatial constraints and interactions among subdivisions of the brain influencing endocranial morphology. Our results suggest that during postnatal development, the relative size changes of supratentorial and infratentorial regions and the cranial base largely constrain brain and endocranium shape. Specifically, a disproportionate increase in the size of the cerebellum relative to the cranial base affects infratentorial spatial packing constraints in neonates, causing inferoposterior expansion of the posterior cranial fossa and coronal reorientation of the petrous bone without lateral opening of the tentorium cerebelli. The dramatic size increase of the cerebellum relative to the cranial base immediately after birth is inferred to be characteristic of human development, which corresponds to previously observed bony shape changes.

evolutionary biology↗

bioRxiv2024

Realized flower constancy in bumble bees: optimal foraging strategy balancing cognitive and travel costs and its possible consequences for floral diversity

O_LIPollinating insects often exhibit flower constancy, i.e., the tendency to make consecutive visits to the same flower species while disregarding others. This behaviour is commonly attributed to the cost of retrieving visual or motor memories from long-term storage while switching between flowers with distinct colours and shapes. Accordingly, researchers often predict co-flowering species to exhibit significantly greater phenotypic diversity than random expectation, thereby minimizing heterospecific pollen transfer. However, field observations have not consistently supported this notion. C_LIO_LIThe observed inconsistencies may arise from variations in travel costs, which depend on the interaction between the foragers constancy level and the spatial mixing of plant species. If species are evenly mixed, constant pollinators incur higher levels of travel cost due to frequent skipping of neighbouring flowers. In contrast, if species are patchily distributed, constant pollinators experience lower levels of travel cost, as most neighbours are of the same species. Considering this, realized flower constancy may be determined as an optimal strategy for balancing cognitive and travel costs, which dynamically vary across different degrees of spatial species mixing. Here we test this possibility in indoor experiments with bumble bees foraging from two differently coloured artificial flowers (species) arranged at three mixing levels. C_LIO_LIFirst, bees dramatically reduced flower constancy as species mixing increased, irrespective of flower spacing. Second, bees were less inclined to switch species after accumulating consecutive visits to one species, suggesting a rapid decay of another species information in short-term memory back to long-term storage. This effect may have additionally contributed to the increased flower constancy observed in species with patchy distributions. Third, bees showed minimal constancy for similarly coloured, evenly mixed flower species, suggesting that these flowers were operated with shared short-term memory. The constancy level was hardly affected by colour similarity when species were patchily distributed. C_LIO_LIResults support our initial hypothesis that realized flower constancy reflects an optimal foraging strategy rather than a fixed outcome of cognitive limitation. Notably, bees constancy increased significantly with greater colour difference only when species were evenly mixed, suggesting a novel perspective: spatial mixing promotes the evolution and maintenance of floral diversity. C_LI

animal behavior and cognition↗

bioRxiv2022

Active site structure of the Shigella flexneri effector OspI

Ubc13 is a critical ubiquitin-conjugating enzyme involved in the nuclear factor-{kappa}B (NF-{kappa}B) signalling pathway. The Shigella flexneri effector OspI targets the host Ubc13 and modifies this enzyme by deamidation of Gln100 into Glu100. This modification inhibits the tumour necrosis factor (TNF) receptor-associated factor 6 (TRAF6)-catalyzed ubiquitination and diacylglycerol-CBM (CARD-Bcl10- Malt1)-TRAF6-NF-{kappa}B signal activation. We have previously reported the wild-type OspI crystal structure, but the catalytic triad does not form the canonical active site. Here, the crystal structure of OspI with a C62S mutation was determined at a resolution of 2.2 [A]. This C62S mutant structure provided the active site conformation with the catalytic site of OspI.

biochemistry↗

bioRxiv2018

PP2AB55δ Responsible for the High Initial Rates of Alcoholic Fermentation in Sake Yeast Strains of Saccharomyces cerevisiae

Sake yeast strain Kyokai no. 7 (K7) and its Saccharomyces cerevisiae relatives carry a homozygous loss-of-function mutation in the RIM15 gene, which encodes a Greatwall-family protein kinase. Disruption of RIM15 in non-sake yeast strains leads to improved alcoholic fermentation, indicating that the defect in Rim15p is associated with the enhanced fermentation performance of sake yeast cells. In order to understand how Rim15p mediates fermentation control, we here focused on target-of-rapamycin protein kinase complex 1 (TORC1) and protein phosphatase 2A with the B55{Delta} regulatory subunit (PP2AB55{delta}), complexes that are known to act upstream and downstream of Rim15p, respectively. Several lines of evidence, including our previous transcriptomic analysis data, suggested enhanced TORC1 signaling in sake yeast cells during sake fermentation. Fermentation tests of the TORC1-related mutants using a laboratory strain revealed that TORC1 signaling positively regulates the initial fermentation rate in a Rim15p-dependent manner. Deletion of the CDC55 gene encoding B55{delta} abolished the high fermentation performance of Rim15p-deficient laboratory yeast and sake yeast cells, indicating that PP2AB55{delta} mediates the fermentation control by TORC1 and Rim15p. The TORC1-Greatwall-PP2AB55{delta} pathway similarly affected the fermentation rate in the fission yeast Schizosaccharomyces pombe, strongly suggested that the evolutionarily conserved pathway governs alcoholic fermentation in yeasts. It is likely that elevated PP2AB55{delta} activity accounts for the high fermentation performance of sake yeast cells. Heterozygous loss-of-function mutations in CDC55 found in K7-related sake strains may indicate that the Rim15p-deficient phenotypes are disadvantageous to cell survival.\n\nIMPORTANCEThe biochemical processes and enzymes responsible for glycolysis and alcoholic fermentation by the yeast S. cerevisiae have long been the subject of scientific research. Nevertheless, the factors determining fermentation performance in vivo are not fully understood. As a result, the industrial breeding of yeast strains has required empirical characterization of fermentation by screening numerous mutants through laborious fermentation tests. To establish a rational and efficient breeding strategy, key regulators of alcoholic fermentation need to be identified. In the present study, we focused on how sake yeast strains of S. cerevisiae have acquired high alcoholic fermentation performance. Our findings provide a rational molecular basis to design yeast strains with optimal fermentation performance for production of alcoholic beverages and bioethanol. In addition, as the evolutionarily conserved TORC1-Greatwall-PP2AB55{delta} pathway plays a major role in the glycolytic control, our work may contribute to research on carbohydrate metabolism in higher eukaryotes.

microbiology↗