Sylvain Hiver, Natsumi Shimizu-Mizuno, Yayoi Ikawa, Eriko Kajikawa, Xiaorei Sai, Hiromi Nishimura, Katsuyoshi Takaoka, Osamu Nishimura, Shigehiro Kuraku, Satoshi Tanaka and Hiroshi Hamada : Gse1, a component of the CoREST complex, is required for placenta development in the mouse, Developmental Biology, 498, 97-105, 2023.
(Summary)
Gse1 is a component of the CoREST complex that acts as an H3K4 and H3K9 demethylase and regulates gene expression. Here, we examined the expression and role of Gse1 in mouse development. Gse1 is expressed in male and female germ cells and plays both maternal and zygotic roles. Thus, maternal deletion of Gse1 results in a high incidence of prenatal death, and zygotic deletion leads to embryonic lethality from embryonic day 12.5 (E12.5) and perinatal death. Gse1 is expressed in the junctional zone and the labyrinth of the developing placenta. Gse1 mutant (Gse1) placenta begins to exhibit histological defects from E14.5, being deficient in MCT4 syncytiotrophoblast II. The number of various cell types was largely maintained in the mutant placenta at E10.5, but several genes were upregulated in giant trophoblasts at E10.5. Placenta-specific deletion of Gse1 with Tat-Cre suggested that defects in Gse1 embryos are due to placental function deficiency. These results suggest that Gse1 is required for placental development in mice, and in turn, is essential for embryonic development.
(Keyword)
Mice / Pregnancy / female / Animals / male / Placentation / Placenta / Embryonic Development / Trophoblasts
Xiaorei Sai, Yayoi Ikawa, Hiromi Nishimura, Katsutoshi Mizuno, Eriko Kajikawa, A Takanobu Katoh, Toshiya Kimura, Hidetaka Shiratori, Katsuyoshi Takaoka, Hiroshi Hamada and Katsura Minegishi : Planar cell polarity-dependent asymmetric organization of microtubules for polarized positioning of the basal body in node cells., Development, 149, 9, 2022.
(Summary)
For left-right symmetry breaking in the mouse embryo, the basal body must become positioned at the posterior side of node cells, but the precise mechanism for this has remained unknown. Here, we examined the role of microtubules (MTs) and actomyosin in this basal body positioning. Exposure of mouse embryos to agents that stabilize or destabilize MTs or F-actin impaired such positioning. Active myosin II was detected at the anterior side of node cells before the posterior shift of the basal body, and this asymmetric activation was lost in Prickle and dachsous mutant embryos. The organization of basal-body associated MTs (baMTs) was asymmetric between the anterior and posterior sides of node cells, with anterior baMTs extending horizontally and posterior baMTs extending vertically. This asymmetry became evident after polarization of the PCP core protein Vangl1 and before the posterior positioning of the basal body, and it also required the PCP core proteins Prickle and dachsous. Our results suggest that the asymmetry in baMT organization may play a role in correct positioning of the basal body for left-right symmetry breaking.
W Gerard Dougherty, Katsutoshi Mizuno, Tabea Nöthe-Menchen, Yayoi Ikawa, Karsten Boldt, Asaf Ta-Shma, Isabella Aprea, Katsura Minegishi, Yuan-Ping Pang, Petra Pennekamp, T Niki Loges, Johanna Raidt, Rim Hjeij, Julia Wallmeier, Huda Mussaffi, Zeev Perles, Orly Elpeleg, Franziska Rabert, Hidetaka Shiratori, J Stef Letteboer, Nicola Horn, Samuel Young, Timo Strünker, Friederike Stumme, Claudius Werner, Heike Olbrich, Katsuyoshi Takaoka, Takahiro Ide, Kyaw Wang Twan, Luisa Biebach, Jörg Große-Onnebrink, A Judith Klinkenbusch, Kavita Praveen, C Diana Bracht, M Inga Höben, Katrin Junger, Jana Gützlaff, Sandra Cindrić, Micha Aviram, Thomas Kaiser, Yasin Memari, P Petras Dzeja, Bernd Dworniczak, Marius Ueffing, Ronald Roepman, Kerstin Bartscherer, Nicholas Katsanis, E Erica Davis, Israel Amirav, Hiroshi Hamada and Heymut Omran : CFAP45 deficiency causes situs abnormalities and asthenospermia by disrupting an axonemal adenine nucleotide homeostasis module., Nature Communications, 11, 1, 2020.
(Summary)
mice is rescued with the addition of either AMP or ADP with ATP, compared to ATP alone. We propose that CFAP45 supports mammalian ciliary and flagellar beating via an adenine nucleotide homeostasis module.
(Keyword)
Adenine Nucleotides / Adolescent / Adult / Animals / Asthenozoospermia / Axoneme / CRISPR-Cas Systems / Cilia / Cytoskeletal Proteins / DNA Mutational Analysis / Disease Models, Animal / Epididymis / Female / Flagella / Humans / Loss of Function Mutation / Male / Mice / Mice, Knockout / Middle Aged / Planarians / Respiratory Mucosa / Situs Inversus / Sperm Motility / Tomography, X-Ray Computed / Whole Exome Sequencing
Nobuyuki Kawamura, Katsuyoshi Takaoka, Hiroshi Hamada, Anna-Katerina Hadjantonakis, Ge-Hong Sun-Wada and Yoh Wada : Rab7-Mediated Endocytosis Establishes Patterning of Wnt Activity through Inactivation of Dkk Antagonism, Cell Reports, 31, 10, 107733, 2020.
(Summary)
Endocytosis has been proposed to modulate cell signaling activities. However, the role of endocytosis in embryogenesis, which requires coordination of multiple signaling inputs, has remained less understood. We previously showed that mouse embryos lacking a small guanosine triphosphate (GTP)-binding protein Rab7 implicated in endocytic flow are defective in gastrulation. Here, we investigate how subcellular defects associated with Rab7 deficiency are related to the observed developmental defects. Rab7-deficient embryos fail to organize mesodermal tissues due to defects in Wnt-β-catenin signaling. Visceral endoderm (VE)-specific ablation of Rab7 results in patterning defects similar to systemic Rab7 deletion. Rab7 mutants accumulate the Wnt antagonist Dkk1 in the extracellular space and in intracellular compartments throughout the VE epithelium. These data indicate that Rab7-dependent endocytosis regulates the concentration and availability of extracellular Dkk1, thereby relieving the epiblast of antagonism. This intercellular mechanism therefore organizes distinct spatiotemporal patterns of canonical Wnt activity during the peri-gastrulation stages of embryonic development.
Katsutoshi Mizuno, Kei Shiozawa, Takanobu A Katoh, Katsura Minegishi, Takahiro Ide, Yayoi Ikawa, Hiromi Nishimura, Katsuyoshi Takaoka, Takeshi Itabashi, Atsuko H Iwane, Junichi Nakai, Hidetaka Shiratori and Hiroshi Hamada : Role of Ca2+ transients at the node of the mouse embryo in breaking of left-right symmetry, Science Advances, 6, 30, 1195, 2020.
(Summary)
Immotile cilia sense extracellular signals such as fluid flow, but whether Ca plays a role in flow sensing has been unclear. Here, we examined the role of ciliary Ca in the flow sensing that initiates the breaking of left-right (L-R) symmetry in the mouse embryo. Intraciliary and cytoplasmic Ca transients were detected in the crown cells at the node. These Ca transients showed L-R asymmetry, which was lost in the absence of fluid flow or the PKD2 channel. Further characterization allowed classification of the Ca transients into two types: cilium-derived, L-R-asymmetric transients (type 1) and cilium-independent transients without an L-R bias (type 2). Type 1 intraciliary transients occurred preferentially at the left posterior region of the node, where L-R symmetry breaking takes place. Suppression of intraciliary Ca transients delayed L-R symmetry breaking. Our results implicate cilium-derived Ca transients in crown cells in initiation of L-R symmetry breaking in the mouse embryo.