Shigeru Iida, Yasumasa Morita, Jeong-Doo Choi, Kyeung-Il Park, Atsushi Hoshino
Among the genus Ipomoea, three morning glories, I. nil (the Japanese morning glory), I. purpurea (the common morning glory), and I. tricolor, were domesticated well for floricultural plants, and many spontaneous mutants displaying various flower pigmentation patterns were isolated. Most of these spontaneous mutations were found to be caused by the insertion of DNA transposable elements in the genes for the anthocyanin pigmentation in flowers, and many of them exhibited variegated flowers, such as white flowers with pigmented spots and sectors. Here, we describe the historical background of the mutants displaying variegated flowers and review the genetic and epigenetic regulation in flower pigmentation associated with transposable elements of these morning glories. The flecked, speckled, r-1, and purple mutations in I. nil were caused by insertions of Tpn1 and its relatives in the En/Spm superfamily, Tpn2, Tpn3, and Tpn4, into the genes for anthocyanin coloration in flowers, i.e., DFR-B, CHI, CHS-D, and InNHX1, respectively. Similarly, the flaked and pink mutants of I. purpurea have distantly related elements, Tip100 and Tip201, in the Ac/Ds superfamily inserted into the CHS-D and F3'H genes, respectively. The flower variegation patterns can be determined by the frequency and timing of the excision of these transposons, and their stable insertions produce plain color flowers without generating pigmented spots or sectors; furthermore, both genetic and epigenetic regulation appeared to play important roles in determining the frequency and timing of the excision of the transposons. However, flower variegation is not always associated with the excision of an integrated DNA transposon from one of the genes for anthocyanin pigmentation. The mutant Flying Saucers of I. tricolor displaying variegated flowers was found to have the transposon ItMULE1 inserted into the DFR-B promoter region, but no excision of ItMULE1 from the DFR-B could be detected in the variegated flower lines. The instable pearly-vrg allele in cv. Flying Saucers is likely to be an epiallele because the DNA methylation in the DFR-B promoter appeared to be associated with flower pigmentation.
{"title":"Genetics and epigenetics in flower pigmentation associated with transposable elements in morning glories.","authors":"Shigeru Iida, Yasumasa Morita, Jeong-Doo Choi, Kyeung-Il Park, Atsushi Hoshino","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Among the genus Ipomoea, three morning glories, I. nil (the Japanese morning glory), I. purpurea (the common morning glory), and I. tricolor, were domesticated well for floricultural plants, and many spontaneous mutants displaying various flower pigmentation patterns were isolated. Most of these spontaneous mutations were found to be caused by the insertion of DNA transposable elements in the genes for the anthocyanin pigmentation in flowers, and many of them exhibited variegated flowers, such as white flowers with pigmented spots and sectors. Here, we describe the historical background of the mutants displaying variegated flowers and review the genetic and epigenetic regulation in flower pigmentation associated with transposable elements of these morning glories. The flecked, speckled, r-1, and purple mutations in I. nil were caused by insertions of Tpn1 and its relatives in the En/Spm superfamily, Tpn2, Tpn3, and Tpn4, into the genes for anthocyanin coloration in flowers, i.e., DFR-B, CHI, CHS-D, and InNHX1, respectively. Similarly, the flaked and pink mutants of I. purpurea have distantly related elements, Tip100 and Tip201, in the Ac/Ds superfamily inserted into the CHS-D and F3'H genes, respectively. The flower variegation patterns can be determined by the frequency and timing of the excision of these transposons, and their stable insertions produce plain color flowers without generating pigmented spots or sectors; furthermore, both genetic and epigenetic regulation appeared to play important roles in determining the frequency and timing of the excision of the transposons. However, flower variegation is not always associated with the excision of an integrated DNA transposon from one of the genes for anthocyanin pigmentation. The mutant Flying Saucers of I. tricolor displaying variegated flowers was found to have the transposon ItMULE1 inserted into the DFR-B promoter region, but no excision of ItMULE1 from the DFR-B could be detected in the variegated flower lines. The instable pearly-vrg allele in cv. Flying Saucers is likely to be an epiallele because the DNA methylation in the DFR-B promoter appeared to be associated with flower pigmentation.</p>","PeriodicalId":50880,"journal":{"name":"Advances in Biophysics","volume":"38 ","pages":"141-59"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24769780","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}
Pub Date : 2004-01-01DOI: 10.1016/S0065-227X(04)80106-0
Takehiko Nohmi, Ken-Ichi Masumura
Human genome is continuously exposed to various DNA damaging agents including reactive oxygen species. Of various forms of DNA damage, double-strand breaks (DSBs) in DNA are the most detrimental because of the mutagenicity and cytotoxicity. To combat the serious threats posed by DSBs, cells evolved various homologous and non-homologous recombination repair mechanisms. However, some repair mechanisms appear to be involved in the induction of genome rearrangements such as deletions. To analyze the deletion mutations in a whole body system, gpt delta mice were established. In this mouse model, deletions in λ, DNA integrated in the chromosome are preferentially selected as Spi− phages, which can then be subjected for molecular analysis. Here, we reported the sequence characteristics of deletions induced by ionizing radiations in the liver, ultraviolet light β in the epidermis, mitomycin C in the bone marrow and heterocyclic amine PhIP in the colon. To our knowledge, this is the first report in which in vivo deletion mutations are systematically analyzed at the molecular level. About half of the large deletions occur between short direct-repeat sequences and the remainder had flush ends, suggesting that they are generated during the repair of DSBs in DNA. The results also suggest that mutation induction and repair mechanisms may vary depending on the type of organs/tissues examined, i.e., germ cells versus somatic cells or highly proliferating cells versus slowly proliferating cells. Possible mechanisms of intrachromosomal deletion mutations are discussed.
{"title":"Gpt delta transgenic mouse: A novel approach for molecular dissection of deletion mutations in vivo","authors":"Takehiko Nohmi, Ken-Ichi Masumura","doi":"10.1016/S0065-227X(04)80106-0","DOIUrl":"10.1016/S0065-227X(04)80106-0","url":null,"abstract":"<div><p>Human genome is continuously exposed to various DNA damaging agents including reactive oxygen species. Of various forms of DNA damage, double-strand breaks (DSBs) in DNA are the most detrimental because of the mutagenicity and cytotoxicity. To combat the serious threats posed by DSBs, cells evolved various homologous and non-homologous recombination repair mechanisms. However, some repair mechanisms appear to be involved in the induction of genome rearrangements such as deletions. To analyze the deletion mutations in a whole body system, <em>gpt</em> delta mice were established. In this mouse model, deletions in λ, DNA integrated in the chromosome are preferentially selected as Spi<sup>−</sup> phages, which can then be subjected for molecular analysis. Here, we reported the sequence characteristics of deletions induced by ionizing radiations in the liver, ultraviolet light β in the epidermis, mitomycin C in the bone marrow and heterocyclic amine PhIP in the colon. To our knowledge, this is the first report in which <em>in vivo</em> deletion mutations are systematically analyzed at the molecular level. About half of the large deletions occur between short direct-repeat sequences and the remainder had flush ends, suggesting that they are generated during the repair of DSBs in DNA. The results also suggest that mutation induction and repair mechanisms may vary depending on the type of organs/tissues examined, <em>i.e.</em>, germ cells versus somatic cells or highly proliferating cells versus slowly proliferating cells. Possible mechanisms of intrachromosomal deletion mutations are discussed.</p></div>","PeriodicalId":50880,"journal":{"name":"Advances in Biophysics","volume":"38 ","pages":"Pages 97-121"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0065-227X(04)80106-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55849805","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}
Pub Date : 2004-01-01DOI: 10.1016/S0065-227X(04)80091-1
Kohji Kusano
Pairing between homologous DNA controls cellular functions including double-strand break repair, mitotic recombination, and progression of DNA replication forks, as well as chiasma formation during meiosis. Here I summarize that homologous interaction could promote the cell killing in bacteria, yeast, and multicellular organisms. The mechanisms of cell killing are categorized into two types: (1) the killing due to the accumulation of extrachromosomal DNA; (2) the killing induced by Holliday junction structures. I propose that the mechanisms of such killing function as novel apoptotic pathways in the cells carrying severe DNA damages to eliminate such damages from cell population.
{"title":"Cell death promoted by homologous DNA interaction from bacteria to humans","authors":"Kohji Kusano","doi":"10.1016/S0065-227X(04)80091-1","DOIUrl":"10.1016/S0065-227X(04)80091-1","url":null,"abstract":"<div><p>Pairing between homologous DNA controls cellular functions including double-strand break repair, mitotic recombination, and progression of DNA replication forks, as well as chiasma formation during meiosis. Here I summarize that homologous interaction could promote the cell killing in bacteria, yeast, and multicellular organisms. The mechanisms of cell killing are categorized into two types: (1) the killing due to the accumulation of extrachromosomal DNA; (2) the killing induced by Holliday junction structures. I propose that the mechanisms of such killing function as novel apoptotic pathways in the cells carrying severe DNA damages to eliminate such damages from cell population.</p></div>","PeriodicalId":50880,"journal":{"name":"Advances in Biophysics","volume":"38 ","pages":"Pages 81-96"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0065-227X(04)80091-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"55849796","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}
Pairing between homologous DNA controls cellular functions including double-strand break repair, mitotic recombination, and progression of DNA replication forks, as well as chiasma formation during meiosis. Here I summarize that homologous interaction could promote the cell killing in bacteria, yeast, and multicellular organisms. The mechanisms of cell killing are categorized into two types: (1) the killing due to the accumulation of extrachromosomal DNA; (2) the killing induced by Holliday junction structures. I propose that the mechanisms of such killing function as novel apoptotic pathways in the cells carrying severe DNA damages to eliminate such damages from cell population.
{"title":"Cell death promoted by homologous DNA interaction from bacteria to humans.","authors":"Kohji Kusano","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Pairing between homologous DNA controls cellular functions including double-strand break repair, mitotic recombination, and progression of DNA replication forks, as well as chiasma formation during meiosis. Here I summarize that homologous interaction could promote the cell killing in bacteria, yeast, and multicellular organisms. The mechanisms of cell killing are categorized into two types: (1) the killing due to the accumulation of extrachromosomal DNA; (2) the killing induced by Holliday junction structures. I propose that the mechanisms of such killing function as novel apoptotic pathways in the cells carrying severe DNA damages to eliminate such damages from cell population.</p>","PeriodicalId":50880,"journal":{"name":"Advances in Biophysics","volume":"38 Complete","pages":"81-96"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40913109","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 frequency of illegitimate recombination has been measured by a lambdabio transducing phage assay during the induction of the E. coli lambda c1857 lysogen. Illegitimate recombination falls into two classes, short homology-independent and short homology-dependent illegitimate recombination. The former involves sequences with virtually no homology, and is mediated by DNA topoisomerases and controlled by the DNA binding protein HU. The latter is induced by UV irradiation or other DNA damaging agents and requires short regions of homology, usually contain 4 to 13 base pairs, at sites involved in recombination. It has been shown that the RecJ exonuclease promotes short homology-dependent illegitimate recombination, but that the RecQ helicase suppresses it. In addition, we have shown that the overexpression of RecE and RecT enhances the frequencies of spontaneous and UV-induced illegitimate recombination and that the RecJ, RecF, RecO, and RecR functions are required for this RecE-mediated illegitimate recombination. Moreover, we have also indicated that RecQ plays a role in the suppression of RecEmediated illegitimate recombination, with the participation of DnaB, Fis, Exol, and H-NS. Models have been proposed for these modes of recombination: the DNA gyrase subunit exchange model for short homology-independent illegitimate recombination and the "double-strand break and join" model for short homologydependent illegitimate recombination. Many features of these models remain to be tested in future studies.
{"title":"Illegitimate recombination mediated by double-strand break and end-joining in Escherichia coli.","authors":"Hideo Ikeda, Kouya Shiraishi, Yasuyuki Ogata","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The frequency of illegitimate recombination has been measured by a lambdabio transducing phage assay during the induction of the E. coli lambda c1857 lysogen. Illegitimate recombination falls into two classes, short homology-independent and short homology-dependent illegitimate recombination. The former involves sequences with virtually no homology, and is mediated by DNA topoisomerases and controlled by the DNA binding protein HU. The latter is induced by UV irradiation or other DNA damaging agents and requires short regions of homology, usually contain 4 to 13 base pairs, at sites involved in recombination. It has been shown that the RecJ exonuclease promotes short homology-dependent illegitimate recombination, but that the RecQ helicase suppresses it. In addition, we have shown that the overexpression of RecE and RecT enhances the frequencies of spontaneous and UV-induced illegitimate recombination and that the RecJ, RecF, RecO, and RecR functions are required for this RecE-mediated illegitimate recombination. Moreover, we have also indicated that RecQ plays a role in the suppression of RecEmediated illegitimate recombination, with the participation of DnaB, Fis, Exol, and H-NS. Models have been proposed for these modes of recombination: the DNA gyrase subunit exchange model for short homology-independent illegitimate recombination and the \"double-strand break and join\" model for short homologydependent illegitimate recombination. Many features of these models remain to be tested in future studies.</p>","PeriodicalId":50880,"journal":{"name":"Advances in Biophysics","volume":"38 Complete","pages":"3-20"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40913752","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}
Pub Date : 2003-01-01DOI: 10.1016/S0065-227X(03)80004-7
Katsuhito Takahashi, Hisako Yamamura
{"title":"Studies and perspectives of calponin in smooth muscle regulation and cancer gene therapy","authors":"Katsuhito Takahashi, Hisako Yamamura","doi":"10.1016/S0065-227X(03)80004-7","DOIUrl":"10.1016/S0065-227X(03)80004-7","url":null,"abstract":"","PeriodicalId":50880,"journal":{"name":"Advances in Biophysics","volume":"37 ","pages":"Pages 91-111"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0065-227X(03)80004-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22559700","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}
Pub Date : 2003-01-01DOI: 10.1016/S0065-227X(03)80003-5
Ryuzo Yanagimachi
{"title":"Fertilization and development initiation in orthodox and unorthodox ways: From normal fertilization to cloning","authors":"Ryuzo Yanagimachi","doi":"10.1016/S0065-227X(03)80003-5","DOIUrl":"10.1016/S0065-227X(03)80003-5","url":null,"abstract":"","PeriodicalId":50880,"journal":{"name":"Advances in Biophysics","volume":"37 ","pages":"Pages 49-89"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0065-227X(03)80003-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22559699","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}
Pub Date : 2003-01-01DOI: 10.1016/S0065-227X(03)80008-4
{"title":"17 Years with Mr. Miyazaki","authors":"","doi":"10.1016/S0065-227X(03)80008-4","DOIUrl":"https://doi.org/10.1016/S0065-227X(03)80008-4","url":null,"abstract":"","PeriodicalId":50880,"journal":{"name":"Advances in Biophysics","volume":"37 ","pages":"Pages 121-122"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0065-227X(03)80008-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92110809","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2003-01-01DOI: 10.1016/S0065-227X(03)80006-0
{"title":"Suggestions to authors","authors":"","doi":"10.1016/S0065-227X(03)80006-0","DOIUrl":"https://doi.org/10.1016/S0065-227X(03)80006-0","url":null,"abstract":"","PeriodicalId":50880,"journal":{"name":"Advances in Biophysics","volume":"37 ","pages":"Pages 117-118"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0065-227X(03)80006-0","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92150053","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}