On 23rd March last, in the city of Granada (Spain), Professor Miguel Guirao-Perez passed away at the age of 85. He founded this journal in 1960 under the title of Anales del Desarrollo (Annals of Development), one of the few periodic publications in the world devoted exclusively to developmental Biology at that time and oriented mainly to descriptive and experimental Embryology and Teratology.
{"title":"In Memoriam - Miguel Guirao (1924-2010)","authors":"J. Aréchaga","doi":"10.1387/IJDB.113284JA","DOIUrl":"https://doi.org/10.1387/IJDB.113284JA","url":null,"abstract":"On 23rd March last, in the city of Granada (Spain), Professor Miguel Guirao-Perez passed away at the age of 85. He founded this journal in 1960 under the title of Anales del Desarrollo (Annals of Development), one of the few periodic publications in the world devoted exclusively to developmental Biology at that time and oriented mainly to descriptive and experimental Embryology and Teratology.","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2010-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82317391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Using time-lapse video recording and comparing successive digital images, we found that 38% of Xenopus laevis embryos (n=118) exhibited rotation during the second cell cycle. This rotation, which we term the second rotation, started approximately during the appearance of the first cleavage furrow and proceeded clockwise or counterclockwise around the vertical axis. Rotations lasted for 5-30 minutes, i.e. up to the beginning of the third cell cycle. The mean rotation angle was 36.4 degrees, with a maximum rotation of 77 degrees. No mortality was observed among the embryos exhibiting rotation. The second rotation was observed to be similar to the well-known fertilization rotation which takes place during the first cell cycle. The possible nature and significance of the second rotation are discussed.
{"title":"Rotation in Xenopus laevis embryos during the second cell cycle.","authors":"S. M. Starodubov, Vladimir A Golychenkov","doi":"10.1387/ijdb.062266ss","DOIUrl":"https://doi.org/10.1387/ijdb.062266ss","url":null,"abstract":"Using time-lapse video recording and comparing successive digital images, we found that 38% of Xenopus laevis embryos (n=118) exhibited rotation during the second cell cycle. This rotation, which we term the second rotation, started approximately during the appearance of the first cleavage furrow and proceeded clockwise or counterclockwise around the vertical axis. Rotations lasted for 5-30 minutes, i.e. up to the beginning of the third cell cycle. The mean rotation angle was 36.4 degrees, with a maximum rotation of 77 degrees. No mortality was observed among the embryos exhibiting rotation. The second rotation was observed to be similar to the well-known fertilization rotation which takes place during the first cell cycle. The possible nature and significance of the second rotation are discussed.","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83474828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The Hedgehog (Hh) family of signalling molecules is essential for a wide range of developmental processes. Mammalian studies have implicated the Hedgehog pathway in the aetiology of anorectal malformations (ARMs), relatively common congenital anomalies caused by failures in the development of the cloaca. In this study we demonstrate that Hh signalling is absolutely required for the formation of the zebrafish cloaca and that the severity of the posterior gut abnormalities induced by a reduction in Hh activity is dependent on the levels of Hh signal transduction. The complete loss of all Hh activity results in the most severe defects and the critical period for Hh activity is between 34 and 74 hours post fertilisation. Using a range of mutant genotypes that cause notochord and floorplate abnormalities, we show that the source of the Hh signals required for posterior gut formation is the endoderm and not the notochord, as previously postulated in mammalian models of ARMs. We show that Adriamycin, a drug known to cause ARMs in rat, but not chick embryos, has no effect on the development of the zebrafish gastrointestinal tract. These studies establish the zebrafish as a model for ARMs, and for the elucidation of other pathways involved in hindgut developmental processes.
{"title":"Hedgehog signalling is required for cloacal development in the zebrafish embryo.","authors":"C. Parkin, C. Allen, P. Ingham","doi":"10.1387/ijdb.082669cp","DOIUrl":"https://doi.org/10.1387/ijdb.082669cp","url":null,"abstract":"The Hedgehog (Hh) family of signalling molecules is essential for a wide range of developmental processes. Mammalian studies have implicated the Hedgehog pathway in the aetiology of anorectal malformations (ARMs), relatively common congenital anomalies caused by failures in the development of the cloaca. In this study we demonstrate that Hh signalling is absolutely required for the formation of the zebrafish cloaca and that the severity of the posterior gut abnormalities induced by a reduction in Hh activity is dependent on the levels of Hh signal transduction. The complete loss of all Hh activity results in the most severe defects and the critical period for Hh activity is between 34 and 74 hours post fertilisation. Using a range of mutant genotypes that cause notochord and floorplate abnormalities, we show that the source of the Hh signals required for posterior gut formation is the endoderm and not the notochord, as previously postulated in mammalian models of ARMs. We show that Adriamycin, a drug known to cause ARMs in rat, but not chick embryos, has no effect on the development of the zebrafish gastrointestinal tract. These studies establish the zebrafish as a model for ARMs, and for the elucidation of other pathways involved in hindgut developmental processes.","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74069019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Salvemini, M. Robertson, B. Aronson, P. Atkinson, L. C. Polito, G. Saccone
In Drosophila melanogaster, transformer-2 (TRA-2) which is a non-sex-specific auxiliary splicing factor, is required to promote female sexual differentiation by interaction with the female-specific TRA. The two proteins positively regulate the splicing of both doublesex (dsx) and fruitless (fru) pre-mRNAs, which in turn regulate phenotypic and behavioural sexual dimorphism. In the Mediterranean fruitfly Ceratitis capitata, the female-specific CcTRA is similarly required not only for Ccdsx splicing, but also to exert a novel autoregulatory function that consists of promoting female-specific splicing of Cctra pre-mRNA. This study reports the isolation and functional analysis of the C. capitata homologue of the Drosophila transformer-2 gene (Cctra-2). Transient RNAi against Cctra-2 during embryonic development causes the full sex reversal of XX flies in adult fertile pseudo-males, as well as changes in the splicing pattern of Cctra, Ccdsx and Ccfruitless (Ccfru). We propose that: 1) Cctra-2, as in Drosophila, is necessary for promoting Ccdsx and putative Ccfru pre-mRNA female-specific splicing and that 2) unlike in Drosophila, Cctra-2 appears to be necessary for establishing female sex determination in early XX embryos and for maintaining the positive feedback regulation of Cctra during development.
{"title":"Ceratitis capitata transformer-2 gene is required to establish and maintain the autoregulation of Cctra, the master gene for female sex determination.","authors":"M. Salvemini, M. Robertson, B. Aronson, P. Atkinson, L. C. Polito, G. Saccone","doi":"10.1387/ijdb.082681ms","DOIUrl":"https://doi.org/10.1387/ijdb.082681ms","url":null,"abstract":"In Drosophila melanogaster, transformer-2 (TRA-2) which is a non-sex-specific auxiliary splicing factor, is required to promote female sexual differentiation by interaction with the female-specific TRA. The two proteins positively regulate the splicing of both doublesex (dsx) and fruitless (fru) pre-mRNAs, which in turn regulate phenotypic and behavioural sexual dimorphism. In the Mediterranean fruitfly Ceratitis capitata, the female-specific CcTRA is similarly required not only for Ccdsx splicing, but also to exert a novel autoregulatory function that consists of promoting female-specific splicing of Cctra pre-mRNA. This study reports the isolation and functional analysis of the C. capitata homologue of the Drosophila transformer-2 gene (Cctra-2). Transient RNAi against Cctra-2 during embryonic development causes the full sex reversal of XX flies in adult fertile pseudo-males, as well as changes in the splicing pattern of Cctra, Ccdsx and Ccfruitless (Ccfru). We propose that: 1) Cctra-2, as in Drosophila, is necessary for promoting Ccdsx and putative Ccfru pre-mRNA female-specific splicing and that 2) unlike in Drosophila, Cctra-2 appears to be necessary for establishing female sex determination in early XX embryos and for maintaining the positive feedback regulation of Cctra during development.","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84528573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
In mice, completion of preimplantation development in vitro is restricted to certain crosses between inbred strains. Most of the outbred and inbred strains cease development at the 2-cell stage, a phenomenon known as the "2-cell block". Reciprocal mating between blocking and non-blocking strains has shown that the 2-cell block is dependent upon female, but not male, developmental information. One question that still remains unanswered is whether the genome of the metaphase II (MII) oocyte is genetically programmed to express, during the very early stages of development, some factor(s) required to determine developmental competence beyond the 2-cell stage. In the present study, we have addressed this question by performing reciprocal MII-chromosome plate transfer between MII oocytes of a non-blocking inbred strain and MII oocytes of a blocking outbred strain. Here, we report that development beyond the 2-cell stage does not depend on the MII genome, but instead it relies on a cytoplasmic factor(s) already present in ovulated non-blocking oocytes, but absent, inactive or quantitatively insufficient in blocking oocytes. Further evidence of the ooplasmic origin of this component(s) was obtained by transferring a small quantity of ooplasm from non-blocking MII oocytes to blocking MII oocytes or 2-cell embryos. Following the transfer, a high percentage of blocking oocytes/embryos acquired developmental competence beyond the 2-cell stage and reached the blastocyst stage. This study shows that development beyond the 2-cell stage relies also on a factor(s) already present in the ovulated oocyte.
{"title":"The 2-cell block occurring during development of outbred mouse embryos is rescued by cytoplasmic factors present in inbred metaphase II oocytes.","authors":"M. Zanoni, S. Garagna, C. Redi, M. Zuccotti","doi":"10.1387/ijdb.082617mz","DOIUrl":"https://doi.org/10.1387/ijdb.082617mz","url":null,"abstract":"In mice, completion of preimplantation development in vitro is restricted to certain crosses between inbred strains. Most of the outbred and inbred strains cease development at the 2-cell stage, a phenomenon known as the \"2-cell block\". Reciprocal mating between blocking and non-blocking strains has shown that the 2-cell block is dependent upon female, but not male, developmental information. One question that still remains unanswered is whether the genome of the metaphase II (MII) oocyte is genetically programmed to express, during the very early stages of development, some factor(s) required to determine developmental competence beyond the 2-cell stage. In the present study, we have addressed this question by performing reciprocal MII-chromosome plate transfer between MII oocytes of a non-blocking inbred strain and MII oocytes of a blocking outbred strain. Here, we report that development beyond the 2-cell stage does not depend on the MII genome, but instead it relies on a cytoplasmic factor(s) already present in ovulated non-blocking oocytes, but absent, inactive or quantitatively insufficient in blocking oocytes. Further evidence of the ooplasmic origin of this component(s) was obtained by transferring a small quantity of ooplasm from non-blocking MII oocytes to blocking MII oocytes or 2-cell embryos. Following the transfer, a high percentage of blocking oocytes/embryos acquired developmental competence beyond the 2-cell stage and reached the blastocyst stage. This study shows that development beyond the 2-cell stage relies also on a factor(s) already present in the ovulated oocyte.","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88526229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Matrix metalloproteinases (MMP) constitute a family of more than 25 enzymes which process a large number of pericellular substrates. Even though initially reported to have an ability to degrade almost all of the extracellular components, MMP are now known to play roles which are not limited to the breakdown of extracellular barriers. In fact, MMPs regulate many biological processes, being involved not only in physiological events, but also in pathological processes. Strikingly, MMPs have been found to be involved in the physiology of the Central Nervous System (CNS), taking part and playing important roles in several processes such as repair and ontogeny, as well as in pathological conditions of the CNS. Initially considered to be a static structure, lacking regenerative capability, the CNS has been considered for a long time to be a system without renewal capabilities. Recently, the discovery of constant neural replacement has changed our way of considering the adult brain, and the finding of the existence of neural stem cells has opened the way to exciting and fascinating perspectives of the CNS. So, could MMPs, originally found during metamorphosis in tadpoles, and now amazingly identified in the CNS, have something to do in neuronal function? In this review we take into consideration the possible roles of two metalloproteinases, MMP-2 and MMP-9, also called gelatinases, in controlling several aspects of CNS organization, including the modulation of neural stem cell properties and the differentiation of their progeny, both under normal and pathophysiological conditions.
{"title":"Neural stem cells at the crossroads: MMPs may tell the way.","authors":"G. Tonti, F. Mannello, E. Cacci, S. Biagioni","doi":"10.1387/ijdb.082573gt","DOIUrl":"https://doi.org/10.1387/ijdb.082573gt","url":null,"abstract":"Matrix metalloproteinases (MMP) constitute a family of more than 25 enzymes which process a large number of pericellular substrates. Even though initially reported to have an ability to degrade almost all of the extracellular components, MMP are now known to play roles which are not limited to the breakdown of extracellular barriers. In fact, MMPs regulate many biological processes, being involved not only in physiological events, but also in pathological processes. Strikingly, MMPs have been found to be involved in the physiology of the Central Nervous System (CNS), taking part and playing important roles in several processes such as repair and ontogeny, as well as in pathological conditions of the CNS. Initially considered to be a static structure, lacking regenerative capability, the CNS has been considered for a long time to be a system without renewal capabilities. Recently, the discovery of constant neural replacement has changed our way of considering the adult brain, and the finding of the existence of neural stem cells has opened the way to exciting and fascinating perspectives of the CNS. So, could MMPs, originally found during metamorphosis in tadpoles, and now amazingly identified in the CNS, have something to do in neuronal function? In this review we take into consideration the possible roles of two metalloproteinases, MMP-2 and MMP-9, also called gelatinases, in controlling several aspects of CNS organization, including the modulation of neural stem cell properties and the differentiation of their progeny, both under normal and pathophysiological conditions.","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89513435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Our knowledge of how bioactive lipids participate during development has been limited principally due to the difficulties of working with lipids. The availability of some of these lipids is regulated by the Lipid phosphate phosphatases (LPPs). The targeted inactivation of Ppap2b, which codes for the isoenzyme Lpp3, has profound developmental defects. Lpp3 deficient embryos die around E9.5 due to extraembryonic vascular defects, making difficult to analyze its participation in later stages of mouse development. To gain some predictive information regarding the possible participation of Lpp3 in later stages of development, we generated a Ppap2b null reporter allele and it was used to establish its expression pattern in E8.5-13.5 embryos. We found that Ppap2b expression during these stages was highly dynamic with significant expression in structures where multiple inductive interactions occur such as the limb buds, mammary gland primordia, heart cushions and valves among others. These observations suggest that Lpp3 expression may play a key role in modulating/integrating multiple signaling pathways during development.
{"title":"Generation of a reporter-null allele of Ppap2b/Lpp3and its expression during embryogenesis.","authors":"D. Escalante-Alcalde, Sara Morales, C. Stewart","doi":"10.1387/ijdb.082745de","DOIUrl":"https://doi.org/10.1387/ijdb.082745de","url":null,"abstract":"Our knowledge of how bioactive lipids participate during development has been limited principally due to the difficulties of working with lipids. The availability of some of these lipids is regulated by the Lipid phosphate phosphatases (LPPs). The targeted inactivation of Ppap2b, which codes for the isoenzyme Lpp3, has profound developmental defects. Lpp3 deficient embryos die around E9.5 due to extraembryonic vascular defects, making difficult to analyze its participation in later stages of mouse development. To gain some predictive information regarding the possible participation of Lpp3 in later stages of development, we generated a Ppap2b null reporter allele and it was used to establish its expression pattern in E8.5-13.5 embryos. We found that Ppap2b expression during these stages was highly dynamic with significant expression in structures where multiple inductive interactions occur such as the limb buds, mammary gland primordia, heart cushions and valves among others. These observations suggest that Lpp3 expression may play a key role in modulating/integrating multiple signaling pathways during development.","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78484416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
H. Nakazaki, Yueh-wei Shen, B. Yun, Anvesh C. Reddy, Anvesh C. Reddy, Varun Khanna, B. Mania‐Farnell, S. Ichi, David G. McLone, T. Tomita, C. Mayanil
Pax3 regulates neural crest cell migration and is critical during neural crest development. TGFbs modify neural crest cell migration and differentiation. TGFbeta2 nullizygous embryos (TGFbeta2(-/-)Pax3(+/+)) display open neural tube and bifid spine, whereas in wild type embryos, the neural tube is closed. In previous work, we have demonstrated that Pax3 regulates TGFbeta2 by directly binding to cis-regulatory elements on its promoter. In this study, we found that the TGFbeta2 nullizygous phenotype can be reversed to the wild type phenotype by down-regulating one allele of Pax3, as in TGFbeta2(-/-)Pax3(+/-) embryos obtained through breeding TGFb2(+/-)Pax3(+/-) mice. The data in this paper suggest that Pax3 and TGFbeta2 interact in a coordinated gene regulatory network, linked by common downstream effector genes, to bring about this phenotypic reversal. Downstream effectors may include Hes1, Ngn2 and Sox9, as well as other genes involved in neuronal differentiation.
{"title":"Transcriptional regulation by Pax3 and TGFbeta2 signaling: a potential gene regulatory network in neural crest development.","authors":"H. Nakazaki, Yueh-wei Shen, B. Yun, Anvesh C. Reddy, Anvesh C. Reddy, Varun Khanna, B. Mania‐Farnell, S. Ichi, David G. McLone, T. Tomita, C. Mayanil","doi":"10.1387/ijdb.082682hn","DOIUrl":"https://doi.org/10.1387/ijdb.082682hn","url":null,"abstract":"Pax3 regulates neural crest cell migration and is critical during neural crest development. TGFbs modify neural crest cell migration and differentiation. TGFbeta2 nullizygous embryos (TGFbeta2(-/-)Pax3(+/+)) display open neural tube and bifid spine, whereas in wild type embryos, the neural tube is closed. In previous work, we have demonstrated that Pax3 regulates TGFbeta2 by directly binding to cis-regulatory elements on its promoter. In this study, we found that the TGFbeta2 nullizygous phenotype can be reversed to the wild type phenotype by down-regulating one allele of Pax3, as in TGFbeta2(-/-)Pax3(+/-) embryos obtained through breeding TGFb2(+/-)Pax3(+/-) mice. The data in this paper suggest that Pax3 and TGFbeta2 interact in a coordinated gene regulatory network, linked by common downstream effector genes, to bring about this phenotypic reversal. Downstream effectors may include Hes1, Ngn2 and Sox9, as well as other genes involved in neuronal differentiation.","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82392180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Birds have a ZZ/ZW sex chromosome system, but the mechanism of sex determination remains unknown. The heterogametic sex is female (ZW) and one hypothesis holds that the W chromosome carries a dominant-acting ovary-determining gene. The strongest candidate ovary-determinant on the W chromosome is HINTW, which encodes an aberrant nucleotide hydrolase enzyme. HINTW is conserved amongst all carinate (flying) birds and it is strongly expressed in the gonads and other tissues of female chicken embryos. This and other lines of circumstantial evidence support the proposal that HINTW is the female-determining gene in birds. However, in vivo gain-of-function or loss-of-function studies have not hitherto been reported to test this hypothesis. We tested the potential role of HINTW by mis-expressing it in genetically male (ZZ) embryos, using the RCASBP avian retroviral vector. Strong, widespread expression was delivered throughout the embryo, including the urogenital system, as assessed by whole mount in situ hybridisation. This expression pattern mimicked that seen in normal ZW females, in which HINTW is widely expressed. Strong mis-expression was observed throughout the gonads of genetic male (ZZ) embryos. However, despite strong HINTW expression, ZZ gonads developed normally as bilateral testes. In tissue sections of ZZ urogenital systems transgenic for HINTW, normal testicular histology was observed. Female (ZW) gonads over-expressing HINTW also developed normally, with normal ovarian structure and left/right asymmetry. These results provide genetic evidence against a dominant role for HINTW in avian sex determination.
{"title":"Genetic evidence against a role for W-linked histidine triad nucleotide binding protein (HINTW) in avian sex determination.","authors":"C. Smith, K. Roeszler, A. Sinclair","doi":"10.1387/ijdb.082742cs","DOIUrl":"https://doi.org/10.1387/ijdb.082742cs","url":null,"abstract":"Birds have a ZZ/ZW sex chromosome system, but the mechanism of sex determination remains unknown. The heterogametic sex is female (ZW) and one hypothesis holds that the W chromosome carries a dominant-acting ovary-determining gene. The strongest candidate ovary-determinant on the W chromosome is HINTW, which encodes an aberrant nucleotide hydrolase enzyme. HINTW is conserved amongst all carinate (flying) birds and it is strongly expressed in the gonads and other tissues of female chicken embryos. This and other lines of circumstantial evidence support the proposal that HINTW is the female-determining gene in birds. However, in vivo gain-of-function or loss-of-function studies have not hitherto been reported to test this hypothesis. We tested the potential role of HINTW by mis-expressing it in genetically male (ZZ) embryos, using the RCASBP avian retroviral vector. Strong, widespread expression was delivered throughout the embryo, including the urogenital system, as assessed by whole mount in situ hybridisation. This expression pattern mimicked that seen in normal ZW females, in which HINTW is widely expressed. Strong mis-expression was observed throughout the gonads of genetic male (ZZ) embryos. However, despite strong HINTW expression, ZZ gonads developed normally as bilateral testes. In tissue sections of ZZ urogenital systems transgenic for HINTW, normal testicular histology was observed. Female (ZW) gonads over-expressing HINTW also developed normally, with normal ovarian structure and left/right asymmetry. These results provide genetic evidence against a dominant role for HINTW in avian sex determination.","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85181262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eukaryotic cells contain multiple intracellular organelles which are structurally and functionally distinct membrane-delimited compartments. Organelles play vital roles in many cellular events in essentially all eukaryotic cells. Although the canonical roles of organelles are well described by classical in vitro studies, little is known about the specific physiological roles of organelles in neurons, which possess extremely polarized cellular structures and have a massive cellular volume compared with most eukaryotic cells. Studies that make use of recently developed genetic and microscopic techniques are currently elucidating the unexpectedly specialized roles of intracellular, membrane-delimited organelles in neuronal morphogenesis and function, and in human disease. Here we review recent advances in understanding the roles of organelles (the ER-Golgi secretory pathway, endosomes and mitochondria) in developing neurons.
{"title":"Organelles in developing neurons: essential regulators of neuronal morphogenesis and function.","authors":"Sayaka Sekine, M. Miura, T. Chihara","doi":"10.1387/ijdb.082618ss","DOIUrl":"https://doi.org/10.1387/ijdb.082618ss","url":null,"abstract":"Eukaryotic cells contain multiple intracellular organelles which are structurally and functionally distinct membrane-delimited compartments. Organelles play vital roles in many cellular events in essentially all eukaryotic cells. Although the canonical roles of organelles are well described by classical in vitro studies, little is known about the specific physiological roles of organelles in neurons, which possess extremely polarized cellular structures and have a massive cellular volume compared with most eukaryotic cells. Studies that make use of recently developed genetic and microscopic techniques are currently elucidating the unexpectedly specialized roles of intracellular, membrane-delimited organelles in neuronal morphogenesis and function, and in human disease. Here we review recent advances in understanding the roles of organelles (the ER-Golgi secretory pathway, endosomes and mitochondria) in developing neurons.","PeriodicalId":94228,"journal":{"name":"The International journal of developmental biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72798893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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