Publications by authors named "Kenta Wada"

The emu (Dromaius novaehollandiae) is a novel poultry species that produces meat, eggs, and fat. Although emus have recently been domesticated, genetic improvements to establish strains have scarcely progressed. In this study, we investigated the relationship between production traits and perilipin 1-encoding gene (PLIN1) polymorphisms in the emus.

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  • The emu is a new poultry species in Japan but suffers from reduced genetic diversity due to inbreeding in commercial farms.
  • Researchers have found potential genetic resources at Tohoku Safari Park and Fuji/Kakegawa Kachoen Garden Park to enhance this diversity, using advanced genotyping techniques.
  • Analysis revealed that TSP emus are ancestral to Okhotsk Emu Farm, while FGP/KGP emus have a unique genetic profile linked to an isolated wild population in eastern Australia, suggesting valuable contributions to both the Japanese emu industry and conservation efforts.
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  • * To address this, the study analyzed the genetic structure of six Japanese emu farms using mitochondrial DNA and microsatellite techniques, finding significant genetic differentiation among populations.
  • * The research identified four distinct genetic groups within these emu populations, providing valuable insights that could help enhance genetic diversity and support population conservation in Japanese farms.
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Fibroblast growth factor 5 (FGF5) is an important molecule required for the transition from anagen to catagen phase of the mammalian hair cycle. We previously reported that Syrian hamsters harboring a 1-bp deletion in the Fgf5 gene exhibit excessive hair growth in males. Herein, we generated Fgf5 mutant mice using genome editing via oviductal nucleic acid delivery (GONAD)/improved GONAD (i-GONAD), an in vivo genome editing system used to target early embryos present in the oviductal lumen, to study gender differences in hair length in mutant mice.

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Characterization of carcass traits and fat quality is important to effectively produce and genetically improve emus. We investigated carcass traits in 309 emus. The meat production of female emus showed a significantly higher value than that of males (P < 0.

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The emu is a useful and new breed of poultry, but their genetic improvement has not advanced yet due to their very recent domestication. Pedigree information is difficult to record because of their complex reproduction system (polyandry). To identify parent-offspring relationships in the emu, parentage test based on polymorphic DNA markers have to be developed.

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  • The study analyzed the mitochondrial DNA of emus in Japan, focusing on their haplotype composition with 109 individuals sequenced in the D-loop region.
  • Researchers identified four substitution sites and three haplotypes (Hap-a, -b, and -c), with Hap-a being the most common among Japanese emus.
  • The findings revealed significant genetic differentiation among populations and suggest that these insights could help conserve genetic resources for the emu industry in Japan.
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C57BL/6J mice have long been studied as a model of age-related hearing loss (ARHL). In C57BL/6J mice, ARHL begins in the high-frequency range at 3 months of age and spreads toward low frequencies by 10 months of age. We previously confirmed that c.

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The emu (Dromaius novaehollandiae) is a useful poultry animal farmed for fat, meat, and eggs. Genetic structure and relationships among farmed emu populations in Japan are unknown and the number of microsatellite markers for genetic analysis of the emu is insufficient. In this study, we isolated 16 microsatellites from the emu genome and developed ten new microsatellite markers.

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Visual impairment leads to a decrease in quality of life. Cataract is the most commonly observed ocular disease in humans that causes vision disorders. The risk factors associated with cataract development include aging, infections, eye injuries, environmental causes, such as radiation and exposure to ultraviolet rays in sunlight, and genetic mutations.

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Outer hair cells (OHCs) are responsible for the amplification of sound, and the death of these cells leads to hearing loss. Although the mechanisms for sound amplification and OHC death have been well investigated, the effects on the cochlea after OHC death are poorly understood. To study the consequences of OHC death, we established an OHC knockout system using a novel mouse model, Prestin-hDTR, which uses the prestin promoter to express the human diphtheria toxin (DT) receptor gene (hDTR).

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We present a robust method called improved-Genome editing via Oviductal Nucleic Acids Delivery (i-GONAD) that delivers CRISPR ribonucleoproteins to E0.7 embryos via in situ electroporation. The method generates mouse models containing single-base changes, kilobase-sized deletions, and knock-ins.

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The Foxe3 mutation, which causes early-onset cataracts, is a recessive mutation found in SJL/J mice. A previous study reported that cataract phenotypes are modified by the genetic background of mouse inbred strains and that the Pde6b mutation, which induced degeneration of the photoreceptor cells, is a strong candidate genetic modifier to accelerate the severity of cataractogenesis of Foxe3 mice. We created congenic mice by transferring a genomic region including the Foxe3 mutation to the B6 genetic background, which does not carry the Pde6b mutation.

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An unconventional myosin encoded by the myosin VI gene (MYO6) contributes to hearing loss in humans. Homozygous mutations of MYO6 result in nonsyndromic profound congenital hearing loss, DFNB37. Kumamoto shaker/waltzer (ksv) mice harbor spontaneous mutations, and homozygous mutants exhibit congenital defects in balance and hearing caused by fusion of the stereocilia.

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Major intrinsic protein of lens fiber (MIP) is one of the proteins essential for maintaining lens transparency while also contributing to dominant cataracts in humans. The Nodai cataract (Nat) mice harbor a spontaneous mutation in Mip and develop early-onset nuclear cataracts. The Nat mutation is a c.

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Transgenic technologies used for creating a desired genomic change in animals involve three critical steps: isolation of fertilized eggs, microinjection of transgenic DNA into them and their subsequent transfer to recipient females. These ex vivo steps have been widely used for over 3 decades and they were also readily adapted for the latest genome editing technologies such as ZFNs, TALENs, and CRISPR/Cas9 systems. We recently developed a method called GONAD (Genome editing via Oviductal Nucleic Acids Delivery) that does not require all the three critical steps of transgenesis and therefore relieves the bottlenecks of widely used animal transgenic technologies.

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Article Synopsis
  • Hair length in mammals is controlled by the hair cycle; disruptions in this cycle can result in abnormal hair growth patterns due to specific gene mutations, like in FGF5.
  • A study of the long-haired Syrian hamster strain (MALC) showed that testosterone affects hair length; castration led to shorter hair, but reintroducing testosterone restored the long-haired phenotype.
  • The identified mutation (Fgf5malc) in MALC affects the hair growth phase, making males have longer hair because of a prolonged growth period influenced by testosterone; this is the first report linking a gene mutation to sexual differences in hair length.
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Microinjection is considered the gold standard technique for delivery of nucleic acids (NAs; transgenes or genome editing tools such as CRISPR/Cas9 systems) into embryos, for creating genetically modified organisms. It requires sophisticated equipment as well as well-trained and highly skilled personnel to perform the micro-injection technique. Here, we describe a novel and simple microinjection-independent technique, called Genome-editing via Oviductal Nucleic Acids Delivery (GONAD).

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Microphthalmia is a severe ocular disorder, and this condition is typically caused by mutations in transcription factors that are involved in eye development. Mice carrying mutations in these transcription factors would be useful tools for defining the mechanisms underlying developmental eye disorders. We discovered a new spontaneous recessive microphthalmos mouse mutant in the Japanese wild-derived inbred strain KOR1/Stm.

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We discovered a new cataract mutation, kfrs4, in the Kyoto Fancy Rat Stock (KFRS) background. Within 1 month of birth, all kfrs4/kfrs4 homozygotes developed cataracts, with severe opacity in the nuclei of the lens. In contrast, no opacity was observed in the kfrs4/+ heterozygotes.

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The coat of a goat, like that of many mammalian species, consists of an outer coat of coarse hairs and an under coat of fine, downy hairs. The coarse guard hairs are produced by primary follicles and the finer cashmere hairs by secondary follicles. We previously reported that hair keratins are components of cashmere hair, and proteomic analysis revealed that their expression is elevated in winter coat hair.

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While the study of phenotypic variation is a central theme in evolutionary biology, the genetic approaches available to understanding this variation are usually limited because of a lack of genomic information in non-model organisms. This study explored the utility of next-generation sequencing (NGS) technologies for studying phenotypic variations between 2 populations of a non-model species, the Hokkai shrimp (Pandalus latirostris; Decapoda, Pandalidae). Before we performed transcriptome analyses using NGS, we examined the genetic and phenotypic differentiation between the populations.

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The Rinshoken cataract (rct) mutation, which causes congenital cataracts, is a recessive mutation found in SJL/J mice. All mutants present with opacity in the lens by 2 months of age. The rct locus was mapped to a 1.

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We determined the complete nucleotide sequence of the mitochondrial genome of the semidomestic red deer (Cervus elaphus) of New Zealand. The genome was 16,357 bp long and contained 13 protein-coding genes, 12SrRNA, 16SrRNA, 22 tRNAs and a D-loop as found in other mammals. Database homology searches showed that the mitochondrial DNA (mtDNA) sequence from the New Zealand semidomestic deer was similar to partial mtDNA sequences from the European, Norwegian (C.

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