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Biology subjects

Suzuki, N.

Publications and source records attributed to Suzuki, N..

4 recordsLinked to original sources

Time calibrated morpho-molecular classification of Nassellaria (Radiolaria)

Nassellaria are marine radiolarian protists belonging to the Rhizaria lineage. Their skeleton, made of opaline silica, exhibit an excellent fossil record, extremely valuable in micro-paleontological studies for paleo-environmental reconstruction. Yet, to date very little is known about the extant diversity and ecology of Nassellaria in contemporary oceans, and most of it is inferred from their fossil record. Here we present an integrative classification of Nassellaria based on taxonomical marker genes (18S and 28S ribosomal DNA) and morphological characteristics obtained by optical and scanning electron microscopy imaging. Our phylogenetic analyses distinguished 11 main morpho-molecular clades relying essentially on the overall morphology of the skeleton and not on internal structures as previously considered. Using fossil calibrated molecular clock we estimated the origin of Nassellaria among radiolarians primitive forms in the Devonian (ca. 420 Ma), that gave rise to living nassellarian groups in the Triassic (ca. 250 Ma), during the biggest diversification event over their evolutionary history. This morpho-molecular framework provides both a new morphological classification easier to identify under light microscopy and the basis for future molecular ecology surveys. Altogether, it brings a new standpoint to improve our scarce understanding of the ecology and worldwide distribution of extant nassellarians.

molecular biology

HERC2 promotes BLM and WRN to suppress G-quadruplex DNA

BLM and WRN are RecQ DNA helicases essential for genomic stability. Here we demonstrate that HERC2, a HECT E3 ligase, is critical for their functions to suppress G-quadruplex (G4) DNA. HERC2 interacts with BLM, WRN, and replication protein A (RPA) complexes during S-phase of the cell cycle. Depletion of HERC2 dissociates RPA from BLM and WRN complexes and significantly increases G4 formation. Triple depletion revealed that HERC2 has an epistatic relationship with BLM and WRN in their G4- suppressing function. In vitro, HERC2 releases RPA onto single-stranded DNA (ssDNA), rather than anchoring onto RPA-coated ssDNA. CRISPR/Cas9-mediated deletion of the catalytic ubiquitin-binding site of HERC2 causes RPA accumulation in the helicase complexes and increases G4, indicating an essential role for E3 activity in G4 suppression. Both HERC2 depletion and E3 inactivation sensitize cells to the G4-interacting compounds, telomestatin and pyridostatin. Overall, HERC2 is a master regulator of G4 suppression and affects the sensitivity of cells to G4 stabilizers.

molecular biology

Cerebellar nuclei neurons dictate growth of the cortex through developmental scaling of presynaptic Purkinje cells

Efficient function of neural systems requires the production of specific cell types in the correct proportions. Here we report that reduction of the earliest born neurons of the cerebellum, excitatory cerebellar nuclei neurons (eCN), results in a subsequent reduction in growth of the cerebellar cortex due to an accompanying loss of their presynaptic target Purkinje cells. Conditional knockout of the homeobox genes En1 and En2 (En1/2) in the rhombic lip-derived eCN and granule cell precursors leads to embryonic loss of a subset of medial eCN and cell non-autonomous and location specific loss of Purkinje cells, with subsequent proportional scaling down of cortex growth. We propose that subsets of eCN dictate the survival of their specific Purkinje cell partners, and in turn sonic hedgehog secreted by Purkinje cells scales the expansion of granule cells and interneurons to produce functional local circuits and the proper folded morphology of the cerebellum.

developmental biology

Age-dependent dormant resident progenitors are stimulated by injury to regenerate Purkinje neurons

Outside of the neurogenic niches of the brain, postmitotic neurons have not been found to undergo efficient regeneration. Here we demonstrate that Purkinje cells (PCs), which are born at midgestation and are crucial for both development and function of cerebellar circuits, are rapidly and fully regenerated following their ablation at birth. New PCs are produced by a previously unidentified progenitor population and support normal cerebellum development. The number of PC progenitors and their regenerative capacity, however, diminish soon after birth, and consequently PCs are poorly replenished when ablated at postnatal day 5. Nevertheless, the PC-depleted cerebella reach a normal size by increasing cell size, but scaling of neuron types is disrupted and cerebellar function is impaired. Our findings thus provide a new paradigm in the field of neuron regeneration by identifying a unipotent neural progenitor that buffers against perinatal brain injury in a stage-dependent process.\n\nOne sentence summaryInjury induces a dormant progenitor population present at birth to regenerate cerebellar neurons in a time-dependent manner.

developmental biology