Biology subjects

Narumi, T.

Publications and source records attributed to Narumi, T..

3 recordsLinked to original sources

bioRxiv2024

LATE MERISTEM IDENTITY2 regulates cuticle formation on the seed surface and influences seed longevity

The seed coat protects the embryo from severe external environment. Like the aerial plant parts, the exterior surface of the seed coat is surrounded by a cuticle consisting of lipid polyesters and wax. However, the protective role of the cuticle in mature seeds has not been characterized. We herein study the transcriptional regulation of cuticle formation on the seed surface, which influences seed longevity. A chimeric repressor of Arabidopsis thaliana R2R3 MYB transcription factor gene LATE MERISTEM IDENTITY2 (LMI2) and a Torenia fournieri ortholog (TfMYBML3) was expressed in A. thaliana and T. fournieri, respectively. These lines and A. thaliana LMI2 T-DNA insertion lines were analyzed for cuticle deficiencies. A. thaliana LMI2 mutants and chimeric repressor lines exhibited a similar cuticle deficiency in immature seeds. Transmission electron microscopy observations, polyester composition analyses, and gene expression investigations revealed that LMI2 plays an essential role in cuticle development in the seed coat epidermis by regulating cutin biosynthesis. The lmi2-2 mutant exhibited shorter seed longevity than the wild-type controls in an accelerated aging test. These results indicate that LMI2 is a key regulator of cuticle formation in the seed coat, and is important for maintaining seed longevity. Significance statementCuticle is well known to have multiple important roles for surviving in the terrestrial environment, but their specific role on the seed coat and transcriptional regulation have not yet been elucidated. Here we show that LATE MERISTEM IDENTITY 2, encoding a transcription factor regulating floral meristem transition, is required for seed cuticle formation and maintaining seed longevity, providing evidence for a link between surface cuticle and seed longevity.

plant biology↗

bioRxiv2022

Fear in action: Fear conditioning and alleviation through body movements

Acquisition of fear memories enhances survival especially when the memories guide defensive movements to minimize harm. Accordingly, fear memories and body movements have tight relationships in animals: Fear memory acquisition results in adapting reactive defense movements, while training active defense movements to avoid threat reduces fear memory. However, evidence in humans is scarce because their movements are typically marginalized in experiments. Here, we tracked participants whole-body motions while they underwent fear conditioning in a virtual 3D space. First, representational similarity analysis of body motions revealed that participants obtained distinct spatiotemporal movement patterns through fear conditioning. Second, subsequent training to actively avoid threats with naturalistic defensive actions led to a long-term (24 hrs) reduction of physiological and embodied conditioned responses, while extinction or vicarious training only transiently reduced the responses followed by their spontaneous return. Together, our results highlight the intrinsic role of body movements in human fear memory functions, suggesting the potential for improving fear memory interventions through embodiment.

neuroscience↗

bioRxiv2019

Role of microRNA-21 in hypertrophic cardiac remodeling

Hypertension is a major public health problem among with aging population worldwide. It causes cardiac remodeling, including hypertrophy and interstitial fibrosis, which leads to development of hypertensive heart disease (HHD). Although microRNA-21 (miR-21) is associated with fibrogenesis in multiple organs, its impact on hypertrophic cardiac remodeling in hypertension is not known. Circulating miR-21 level was higher in patients with HHD than that in the control subjects. It also positively correlated with serum myocardial fibrotic markers. MiR-21 expression levels were significantly upregulated in the mice hearts after angiotensin II (Ang II) infusion or transverse aortic constriction (TAC) compared with control mice. Expression level of programmed cell death 4 (PDCD4), a main target of miR-21, was significantly decreased in Ang II infused mice and TAC mice compared with control mice. Expression levels of transcriptional activator protein 1 (AP-1) and transforming growth factor-{beta}1 (TGF-{beta}1), which were downstream targets of PDCD4, were increased in Ang II infused mice and TAC mice compared with control mice. In vitro, mirVana-miR-21-specific inhibitor attenuated Ang II-induced PDCD4 downregulation and contributed to subsequent deactivation of AP-1/TGF-{beta}1 signaling pathway in neonatal rat cardiomyocytes. Thus, suppression of miR-21 prevents hypertrophic cardiac remodeling by regulating PDCD4, AP-1, and TGF-{beta}1 signaling pathway.

molecular biology↗