The Experts below are selected from a list of 255 Experts worldwide ranked by ideXlab platform
Masayuki Yamamoto - One of the best experts on this subject based on the ideXlab platform.
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trna production links nutrient conditions to the onset of Sexual Differentiation through the torc1 pathway
EMBO Reports, 2018Co-Authors: Yoko Otsubo, Tomohiko Matsuo, Akiko Nishimura, Masayuki Yamamoto, Akira YamashitaAbstract:Abstract Target of rapamycin (TOR) kinase controls cell growth and metabolism in response to nutrient availability. In the fission yeast Schizosaccharomyces pombe, TOR complex 1 (TORC1) promotes vegetative growth and inhibits Sexual Differentiation in the presence of ample nutrients. Here, we report the isolation and characterization of mutants with similar phenotypes as TORC1 mutants, in that they initiate Sexual Differentiation even in nutrient‐rich conditions. In most mutants identified, TORC1 activity is downregulated and the mutated genes are involved in tRNA expression or modification. Expression of tRNA precursors decreases when cells undergo Sexual Differentiation. Furthermore, overexpression of tRNA precursors prevents TORC1 downregulation upon nitrogen starvation and represses the initiation of Sexual Differentiation. Based on these observations, we propose that tRNA precursors operate in the S. pombe TORC1 pathway to switch growth mode from vegetative to reproductive.
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signaling pathways for fission yeast Sexual Differentiation at a glance
Journal of Cell Science, 2012Co-Authors: Yoko Otsubo, Masayuki YamamotoAbstract:Cellular Differentiation is controlled largely by specific gene expression programs. In the fission yeast Schizosaccharomyces pombe , the high mobility group (HMG) protein Ste11 is the main transcription factor responsible for the switch from cellular proliferation to Sexual Differentiation ([
Yoko Otsubo - One of the best experts on this subject based on the ideXlab platform.
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trna production links nutrient conditions to the onset of Sexual Differentiation through the torc1 pathway
EMBO Reports, 2018Co-Authors: Yoko Otsubo, Tomohiko Matsuo, Akiko Nishimura, Masayuki Yamamoto, Akira YamashitaAbstract:Abstract Target of rapamycin (TOR) kinase controls cell growth and metabolism in response to nutrient availability. In the fission yeast Schizosaccharomyces pombe, TOR complex 1 (TORC1) promotes vegetative growth and inhibits Sexual Differentiation in the presence of ample nutrients. Here, we report the isolation and characterization of mutants with similar phenotypes as TORC1 mutants, in that they initiate Sexual Differentiation even in nutrient‐rich conditions. In most mutants identified, TORC1 activity is downregulated and the mutated genes are involved in tRNA expression or modification. Expression of tRNA precursors decreases when cells undergo Sexual Differentiation. Furthermore, overexpression of tRNA precursors prevents TORC1 downregulation upon nitrogen starvation and represses the initiation of Sexual Differentiation. Based on these observations, we propose that tRNA precursors operate in the S. pombe TORC1 pathway to switch growth mode from vegetative to reproductive.
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signaling pathways for fission yeast Sexual Differentiation at a glance
Journal of Cell Science, 2012Co-Authors: Yoko Otsubo, Masayuki YamamotoAbstract:Cellular Differentiation is controlled largely by specific gene expression programs. In the fission yeast Schizosaccharomyces pombe , the high mobility group (HMG) protein Ste11 is the main transcription factor responsible for the switch from cellular proliferation to Sexual Differentiation ([
Margaret M Mccarthy - One of the best experts on this subject based on the ideXlab platform.
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Sexual Differentiation of the Mammalian Brain
Hormones and Reproduction of Vertebrates, 2020Co-Authors: Desiree L. Krebs-kraft, Margaret M MccarthyAbstract:Publisher Summary This chapter reviews the role of apoptosis, cell genesis, and synaptogenesis in establishing neuroanatomical sex differences. Sexual Differentiation of the mammalian brain requires the activity of gonadal hormones. The organizational/activational hypothesis of Sexual Differentiation postulates that the organizational effects of these gonadal hormones on brain development occur early in life, during a sensitive period, whereas activational effects in adulthood ensure appropriate and timely sex-specific behaviors. Testosterone (T), or estradiol (E 2 ) produced by aromatization of T, is responsible for masculinization of the brain and the expression of normal male reproductive behavior in adulthood. In the absence of early exposure to gonadal hormones, the brain is, by default, feminized and mediates normal female reproductive behavior in adulthood.
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Sexual Differentiation of the brain in man and animals: of relevance to Klinefelter syndrome?
American Journal of Medical Genetics Part C-seminars in Medical Genetics, 2013Co-Authors: Margaret M MccarthyAbstract:The developing brain is highly sensitive to the organizing effects of steroids of gonadal origin in a process referred to as Sexual Differentiation. Early hormone effects prime the brain for adult sensitivity to the appropriate hormonal milieu, maximizing reproductive fitness via coordinated physiology and behavior. Animal models, in particular rodents, have provided insight into general principles and the cellular and molecular mechanisms of brain Differentiation. Cellular endpoints influenced by steroids in the developing brain include neurogenesis, migration, apoptosis, dendritic growth, and synaptic patterning. Important roles for prostaglandins, endocanabinoids, and epigenetics are among the many cellular mediators of hormonal organization. Transference of general principles of brain Sexual Differentiation to humans relies on observations of individuals with genetic anomalies that either increase or decrease hormone exposure and sensitivity. The physiology and behavior of individuals with XXY (Klinefelter syndrome) has not been considered in the context of Sexual Differentiation of the brain, most likely due to the delay in diagnoses and highly variable presentation. The behavioral phenotype and impairments in the domains of speech and language that are characteristic of individuals with XXY is consistent with the reduced androgen production associated with the syndrome. Hormone replacement appears effective in restoring some deficits and impact may be further improved by increased understanding of the hormonally mediated Sexual Differentiation of the brain. 2013 Wiley Periodicals, Inc.
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Sexual Differentiation of the brain in man and animals: of relevance to Klinefelter syndrome?
American journal of medical genetics. Part C Seminars in medical genetics, 2013Co-Authors: Margaret M MccarthyAbstract:The developing brain is highly sensitive to the organizing effects of steroids of gonadal origin in a process referred to as Sexual Differentiation. Early hormone effects prime the brain for adult sensitivity to the appropriate hormonal milieu, maximizing reproductive fitness via coordinated physiology and behavior. Animal models, in particular rodents, have provided insight into general principles and the cellular and molecular mechanisms of brain Differentiation. Cellular endpoints influenced by steroids in the developing brain include neurogenesis, migration, apoptosis, dendritic growth, and synaptic patterning. Important roles for prostaglandins, endocanabinoids, and epigenetics are among the many cellular mediators of hormonal organization. Transference of general principles of brain Sexual Differentiation to humans relies on observations of individuals with genetic anomalies that either increase or decrease hormone exposure and sensitivity. The physiology and behavior of individuals with XXY (Klinefelter syndrome) has not been considered in the context of Sexual Differentiation of the brain, most likely due to the delay in diagnoses and highly variable presentation. The behavioral phenotype and impairments in the domains of speech and language that are characteristic of individuals with XXY is consistent with the reduced androgen production associated with the syndrome. Hormone replacement appears effective in restoring some deficits and impact may be further improved by increased understanding of the hormonally mediated Sexual Differentiation of the brain.
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Reframing Sexual Differentiation of the brain
Nature Neuroscience, 2011Co-Authors: Margaret M Mccarthy, Arthur P. ArnoldAbstract:In the twentieth century, the dominant model of Sexual Differentiation stated that genetic sex (XX versus XY) causes Differentiation of the gonads, which then secrete gonadal hormones that act directly on tissues to induce sex differences in function. This serial model of Sexual Differentiation was simple, unifying and seductive. Recent evidence, however, indicates that the linear model is incorrect and that sex differences arise in response to diverse sex-specific signals originating from inherent differences in the genome and involve cellular mechanisms that are specific to individual tissues or brain regions. Moreover, sex-specific effects of the environment reciprocally affect biology, sometimes profoundly, and must therefore be integrated into a realistic model of Sexual Differentiation. A more appropriate model is a parallel-interactive model that encompasses the roles of multiple molecular signals and pathways that differentiate males and females, including synergistic and compensatory interactions among pathways and an important role for the environment. In this review, the authors discuss the ways in which brain sex difference may arise and provides a model in which genes, hormones and environment can influence the Sexual dimorphism of the brain.
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Evidence for Sexual Differentiation of glia in rat brain.
Hormones and Behavior, 1996Co-Authors: Jessica A. Mong, Rachel L. Kurzweil, Aline M. Davis, Meredith S. Rocca, Margaret M MccarthyAbstract:Abstract It is well established that gonadal steroids mediate Sexual Differentiation of the brain via direct effects on neurons during a restricted critical period. In addition, estrogen can influence glial morphology in the adult brain, andin vitrostudies suggest estrogen induces glial Differentiation. However, there is a lack ofin vivoevidence for steroid effects on glia during the critical period. We report here a hormone-mediated Sexual Differentiation of arcuate glia as early as Postnatal Day 1. Using glial fibrillary acidic protein immunoreactivity (GFAP-ir), we compared the responsiveness of astroglia in the rat arcuate nucleus among five hormonally different groups. The results indicate increased GFAP-ir cell surface area 24 hr after hormonal manipulation in castrate males compared to intact males, intact females (ANOVA;P
Akira Yamashita - One of the best experts on this subject based on the ideXlab platform.
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trna production links nutrient conditions to the onset of Sexual Differentiation through the torc1 pathway
EMBO Reports, 2018Co-Authors: Yoko Otsubo, Tomohiko Matsuo, Akiko Nishimura, Masayuki Yamamoto, Akira YamashitaAbstract:Abstract Target of rapamycin (TOR) kinase controls cell growth and metabolism in response to nutrient availability. In the fission yeast Schizosaccharomyces pombe, TOR complex 1 (TORC1) promotes vegetative growth and inhibits Sexual Differentiation in the presence of ample nutrients. Here, we report the isolation and characterization of mutants with similar phenotypes as TORC1 mutants, in that they initiate Sexual Differentiation even in nutrient‐rich conditions. In most mutants identified, TORC1 activity is downregulated and the mutated genes are involved in tRNA expression or modification. Expression of tRNA precursors decreases when cells undergo Sexual Differentiation. Furthermore, overexpression of tRNA precursors prevents TORC1 downregulation upon nitrogen starvation and represses the initiation of Sexual Differentiation. Based on these observations, we propose that tRNA precursors operate in the S. pombe TORC1 pathway to switch growth mode from vegetative to reproductive.
Arthur P. Arnold - One of the best experts on this subject based on the ideXlab platform.
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Reframing Sexual Differentiation of the brain
Nature Neuroscience, 2011Co-Authors: Margaret M Mccarthy, Arthur P. ArnoldAbstract:In the twentieth century, the dominant model of Sexual Differentiation stated that genetic sex (XX versus XY) causes Differentiation of the gonads, which then secrete gonadal hormones that act directly on tissues to induce sex differences in function. This serial model of Sexual Differentiation was simple, unifying and seductive. Recent evidence, however, indicates that the linear model is incorrect and that sex differences arise in response to diverse sex-specific signals originating from inherent differences in the genome and involve cellular mechanisms that are specific to individual tissues or brain regions. Moreover, sex-specific effects of the environment reciprocally affect biology, sometimes profoundly, and must therefore be integrated into a realistic model of Sexual Differentiation. A more appropriate model is a parallel-interactive model that encompasses the roles of multiple molecular signals and pathways that differentiate males and females, including synergistic and compensatory interactions among pathways and an important role for the environment. In this review, the authors discuss the ways in which brain sex difference may arise and provides a model in which genes, hormones and environment can influence the Sexual dimorphism of the brain.
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Genetically Triggered Sexual Differentiation of Brain and Behavior
Hormones and Behavior, 1996Co-Authors: Arthur P. ArnoldAbstract:Abstract The dominant theory of Sexual Differentiation of the brain holds that sex differences in brain anatomy and function arise because of the action of gonadal steroids during embryonic and neonatal life. In mammals, testicular steroids trigger masculine patterns of neural development, and feminine patterns of neural development occur in the absence of such testicular secretions. In contrast, gonadal Differentiation in mammals is not initiated by hormonal mechanisms, but is regulated by the action of gene products such as SRY, a testis-determining gene on the Y chromosome. This paper argues that such genetic, nonhormonal signals may also trigger specific examples of Sexual Differentiation of the brain. This thesis is supported by two arguments. The first is that “direct genetic” (i.e., nonhormonal) control of Sexual Differentiation may be as likely to evolve as hormonal control. The second line of argument is that neural and nonneural dimorphisms have already been described that are not well explained by classical theories of steroid-dependent Sexual Differentiation and for which other factors need to be invoked.
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Sexual Differentiation of the Brain in Songbirds
Developmental Neuroscience, 1996Co-Authors: Arthur P. Arnold, Juli Wade, William Grisham, Erin C. Jacobs, Anthony T. CampagnoniAbstract:The brain regions that control song in zebra finches are much larger in males, who sing, than in females, who do not. Two major theories have been proposed to explain Sexual Differentiation of the neu
