Biology subjects

MORITA, M.

Publications and source records attributed to MORITA, M..

3 recordsLinked to original sources

bioRxiv2025

The MpCAFA gene encodes a ciliary protein required for spermatozoid motility in the liverwort Marchantia polymorpha

Bryophytes, pteridophytes, and some gymnosperm species produce motile ciliated spermatozoids that navigate to the egg by regulating ciliary motility in response to a concentration gradient of attractants released from the egg and/or the surrounding cells. However, the structural components of spermatozoid cilia in land plants remain largely unknown. In this study, we investigated MpCAFA (combined calcyphosine [CAPS] with flagellar-associated protein 115 [FAP115]; Mp1g04120) in the liverwort Marchantia polymorpha. The N-terminal and near C-terminal regions of MpCAFA showed similarity to CAPS, a mammalian EF-hand protein, and FAP115, a ciliary protein of the green alga Chlamydomonas reinhardtii, respectively. MpCAFA was expressed specifically in antheridia and its orthologs were found in some algae, bryophytes, pteridophytes, and some gymnosperms, but not in most seed plants. Spermatozoids from mutants lacking functional MpCAFA exhibited a significant decrease in swimming speed. Notably, these mutants showed no obvious morphological defects, including a 9 + 2 axoneme arrangement, and retained chemotactic capability and fertility, forming normal spores. This suggests that MpCAFA is required for spermatozoid motility, but not for sperm chemotaxis or subsequent reproductive processes. The introduction of MpCAFApro:MpCAFA-mCitrine fully complemented the mutant phenotype and revealed that MpCAFA-mCitrine was localized along the lengths of the two spermatozoid cilia. Both the CAPS-like and FAP115-like domains were essential for MpCAFA function and subcellular localization in spermatozoid, whereas the C-terminal proline-rich region was dispensable. These findings indicate that MpCAFA is a major ciliary protein in land plants and can serve as a marker for visualizing spermatozoid ciliary movements.

plant biology↗

bioRxiv2024

Glial scar formation by reactive astrocytes derived from oligodendrocyte progenitor cells after closed-head injury

The diversity of reactive astrocytes is key to understanding complicated pathological processes in the brain. The accumulation of reactive astrocytes expressing the neural stem/precursor cell marker Nestin is common after brain injury, but the pathological implications of this reactive astrocyte subpopulation remain elusive. This study initially aimed to determine the origin and fate of these reactive astrocytes expressing Nestin by characterizing cells labeled with green fluorescent protein (GFP) after closed-head injury, using a Nestin promoter region widely utilized to study neural stem/precursor cells. Unexpectedly, oligodendrocyte progenitor cells (OPCs), rather than astrocytes, were robustly and selectively labeled with GFP. A fraction of these cells showed a subsequent upregulation of astrocyte markers and were incorporated into glial scars. These glial scars are aggregates of reactive astrocytes that form between lesion cores and the perilesional recovering region. Deletion of the Stat3 gene, which is essential for astrocyte activation, using a Nestin promoter reduced glial scars, further confirming that OPCs are involved in glial scar formation. Reactive astrocytes labeled with a glial fibrillary acidic protein promoter differed in morphology and distribution from astrocytes derived from OPCs. This confirms that astrocytes and OPCs produce distinct reactive astrocyte subpopulations. Some GFP-labeled OPCs lacking astrocyte markers were found to distribute in perilesional recovering regions. The reduced expression of Nestin and OPC markers in these non-astrocytic descendants of OPCs, coupled with a significant fraction of these cells remaining olig2-positive, suggests that OPCs give rise to both reactive astrocytes and oligodendrocytes. These findings suggest that OPCs are activated by a novel process after brain injury.

neuroscience↗

bioRxiv2022

Cortical-wide impairment of glymphatic system after focal brain injury

In peripheral tissues, cells are maintained in the interstitial fluid that flows from capillaries to lymph system. However, the brain has no lymphatic capillaries, and the actual state of the interstitial fluid has long been unknown. Recently, a glymphatic system has been proposed in which part of the cerebrospinal fluid flowing on the surface of brain tissue enters the brain parenchyma via the peri-arterial space, becomes interstitial fluid, and then flows out again from the peri-venous space. Brain injury due to head contusion or stroke is thought to impair the intracerebral circulation and aggravate the extracellular environment, but the actual situation is unknown. Therefore, in this study, we examined the effects of focal brain tissue damage on intracerebral circulation using the light-injured mouse, an originally developed closed head injury model. In light-injured mice, the injury-making process does not affect intracerebral circulation because the cranium is maintained. However, this method has quantitative problems, so we developed a method to image cerebrospinal fluid and blood vessels from the surface of the cerebral cortex. After examining different injury sites and different time periods after injury, it was found that intracerebral circulation was reduced to the same extent on the ipsilateral and contralateral sides of the injury at one-week post-injury. This intracerebral circulatory deficit was still partially present at four-weeks post-injury. These results indicate that the intracerebral circulation is extensively impaired by local injury and neurodegenerative diseases.

neuroscience↗