Biology subjects

Yamada, J.

Publications and source records attributed to Yamada, J..

5 recordsLinked to original sources

bioRxiv2026

Identity-state expression and switching in co-conscious dissociative identity disorder: a non-traumatic proof-of-concept fMRI study

Dissociative identity disorder (DID) remains debated because identity-state phenomena are privately experienced and may be attributed to suggestion, simulation or role enactment. Most neuroimaging studies rely on symptom provocation or traumatic recall, which complicates interpretation and is poorly suited to co-conscious presentations where simultaneous awareness should make state differences hardest to detect. We applied Identity-State Characterization and Analysis (ID-SCAN), a non-traumatic, identity-cued functional magnetic resonance imaging protocol, to a DSM-5-diagnosed woman with persistent co-consciousness between Adult and Adolescent identity-states. One task used identical insect images that evoked opposite preferences across identity-states; the other used trait judgments about self, the other identity-state and a shared intimate other. Analyses combined Bayesian single-case general linear modelling, generalized psychophysiological interaction connectivity and searchlight representational similarity analysis. Identity-instruction cue epochs were pooled across tasks to assess switch direction. The same insect stimuli engaged different valuation-related configurations across identity-states: Adolescent-selective effects centred on striato-thalamic regions, whereas Adult-selective effects extended to amygdala and orbitofrontal/medial prefrontal cortex, with distinct task-evoked coupling. Adult-as-self and Adolescent-as-self occupied separable positions within canonical self-referential regions. Cue-locked activity differed by switch direction across tasks, with larger reconfiguration when switching to Adult (mean between-cluster beta separation 4.30 versus 0.85; permutation p = 0.0001). Cross-task overlap localized a limited shared task-related substrate mainly to posterior visual and dorsal parietal cortex. Even under persistent co-consciousness and without trauma provocation, identity-state expression and switching showed convergent within-person neural signatures. The findings support non-traumatic mechanistic phenotyping of dissociative presentations and motivate cohort and longitudinal studies, including treatment-tracking work.

neuroscience↗

bioRxiv2024

Association Between Relational Mobility and DNA Methylation in Oxytocin Receptor Gene: A Social Epigenetic Study

DNA methylation is a type of epigenetic modification known to exhibit fluctuations in response to environmental factors. The association of macrosocial factors, such as interpersonal mobility, on methylation has seldom been investigated. This study aimed to examine the association of relational mobility, defined as the extent to which individuals can form and replace social relationships, on the DNA methylation of oxytocin receptor genes. DNA was extracted from the buccal cells of 95 adult participants (50 men and 45 women) and subjected to microarray analysis of DNA methylation using Illumina EPIC v2.0. The findings indicate that the oxytocin receptor genes methylation level was higher in individuals residing in low relational mobility social environments. The CpG site associated with relational mobility is an enhancer region, indicating that social environments with low relational mobility exert a suppressive effect on the transcriptional efficiency of the oxytocin receptor gene. Significance StatementThe association between DNA methylation of the oxytocin receptor gene and relational mobility was examined in 95 adults in their 20s to 60s, and found that those living in social environments with lower levels of relationship mobility had higher rates of DNA methylation of the oxytocin receptor gene. This study is a novel approach to a problem discussed in the social sciences using new analytical techniques in epigenomics.

genetics↗

bioRxiv2021

Dominant Awn Inhibitor, which encodes an ALOG protein in sorghum, suppresses awn formation in rice

The awn, a needle-like structure extending from the tip of the lemma in grass species, plays a role in environmental adaptation and fitness. In some crops, awns appear to have been eliminated during domestication. Although numerous genes involved in awn development have been identified, several dominant genes that eliminate awns are also known to exist. For example, in sorghum (Sorghum bicolor), the dominant awn inhibiting gene has been known since 1921; however, its molecular features remain uncharacterized. In this study, we conducted quantitative trait locus analysis and a genome-wide association study of awn-related traits in sorghum and identified DOMINANT AWN INHIBITOR (DAI), which encodes the ALOG family protein on chromosome 3. DAI appeared to be present in most awnless sorghum cultivars, likely because of its effectiveness. Detailed analysis of the ALOG protein family in cereals revealed that DAI originated from duplication of its twin paralog (DAIori) on chromosome 10. Observations of immature awns in near-isogenic lines revealed that DAI inhibits awn elongation by suppressing both cell proliferation and elongation. We also found that only DAI gained a novel function to inhibit awn elongation through an awn-specific expression pattern distinct from that of DAIori. Interestingly, heterologous expression of DAI with its own promoter in rice inhibited awn elongation in the awned cultivar Kasalath. We found that DAI originated from gene duplication, providing an interesting example of gain-of-function that occurs only in sorghum but shares its functionality with rice and sorghum.

plant biology↗

bioRxiv2021

Genome-wide CRISPRi screening identifies OCIAD1 as a prohibitin client and regulatory determinant of mitochondrial Complex III assembly in human cells

Dysfunction of the mitochondrial electron transport chain (mETC) is a major cause of human mitochondrial diseases. To identify determinants of mETC function, we screened a genome-wide human CRISPRi library under oxidative metabolic conditions with selective inhibition of mitochondrial Complex III and identified OCIA domain-containing protein 1 (OCIAD1) as a Complex III assembly factor. We find that OCIAD1 is an inner mitochondrial membrane protein that forms a complex with supramolecular prohibitin assemblies. Our data indicate that OCIAD1 is required for maintenance of normal steady state levels of Complex III and the proteolytic processing of the catalytic subunit cytochrome c1 (CYC1). In OCIAD1 depleted mitochondria, unprocessed CYC1 is hemylated and incorporated into Complex III. We propose that OCIAD1 acts as an adaptor within prohibitin assemblies to stabilize and/or chaperone CYC1 and to facilitate its proteolytic processing by the IMMP2L protease.

cell biology↗

bioRxiv2021

TRF2-mediated ORC recruitment underlies telomere stability upon DNA replication stress

Telomeres are intrinsically difficult-to-replicate regions of eukaryotic chromosomes. Telomeric repeat binding factor 2 (TRF2) binds to origin recognition complex (ORC) to facilitate the loading of ORC and the replicative helicase MCM complex onto DNA at telomeres. However, the biological significance of the TRF2-ORC interaction for telomere maintenance remains largely elusive. Here, we employed a separation-of-function TRF2 mutant with mutations in two acidic acid residues (E111A and E112A) that specifically inhibited the TRF2-ORC interaction in human cells without substantially inhibiting TRF2 interactions with its other binding partners. The TRF2 mutant was impaired in ORC recruitment to telomeres and showed increased replication stress-associated telomeric DNA damage and telomere instability. Furthermore, overexpression of an ORC1 fragment (amino acids 244-511), which competitively inhibited the TRF2-ORC interaction, increased telomeric DNA damage under replication stress conditions in human cells. Taken together, these findings suggest that TRF2-mediated ORC recruitment contributes to the suppression of telomere instability.

cell biology↗