{"created":"2023-06-20T13:20:58.989114+00:00","id":1058,"links":{},"metadata":{"_buckets":{"deposit":"7e251c17-d1c4-4b8e-8076-07c6a3c637d7"},"_deposit":{"created_by":1,"id":"1058","owners":[1],"pid":{"revision_id":0,"type":"depid","value":"1058"},"status":"published"},"_oai":{"id":"oai:ir.soken.ac.jp:00001058","sets":["2:430:21"]},"author_link":["0","0","0"],"item_1_creator_2":{"attribute_name":"著者名","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"藤倉, 潮"}],"nameIdentifiers":[{}]}]},"item_1_creator_3":{"attribute_name":"フリガナ","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"フジクラ, ウシオ"}],"nameIdentifiers":[{}]}]},"item_1_date_granted_11":{"attribute_name":"学位授与年月日","attribute_value_mlt":[{"subitem_dategranted":"2007-03-23"}]},"item_1_degree_grantor_5":{"attribute_name":"学位授与機関","attribute_value_mlt":[{"subitem_degreegrantor":[{"subitem_degreegrantor_name":"総合研究大学院大学"}]}]},"item_1_degree_name_6":{"attribute_name":"学位名","attribute_value_mlt":[{"subitem_degreename":"博士（理学）"}]},"item_1_description_12":{"attribute_name":"要旨","attribute_value_mlt":[{"subitem_description":"Leaf development relies on cell proliferation, post-mitotic cell expansion and the coordination of  these processes. In several mutants of Arabidopsis thaliana impaired in cell proliferation, such as angustifolia3 (an3), leaf cells at their maturity are larger than those in wide-type leaves. Similar phenotypes have been reported in several mutants or transgenic plants in Oryza sativa and Nicotiana tabacum. These reports have suggested that magnitude of cell expansion is affected by cell proliferation activity during leaf development. This phenomenon, compensation, suggests the presence of coordination between cell proliferation and post-mitotic cell expansion during leaf development. However, knowledge about the oompensation was superficial and the mechanism(s) underlying compensation was unclear. The aim of his Ph.D. thesis is to elucidate the genetic framework that mediates compensation. To this end, he focused on an3 as a model case of compensation, since an3 is one of the best characterized compensation-exhibiting mutants. <br />        Since compensation consists of two different events, namely, the reduction in Cell number and the increase in cell size, he hypothesized that compensation can be theoretically separated into two distinct processes based on developmental processes; the induction process, which involves the reduction of cell proliferation; and the response process, during which cell expansion is enhanced. The originality in his Ph.D. thesis is that he investigated separately these two processes: induction and response of compensation. He adopted a strategy to genetically dissect the compensation syndrome using knowledge on anatomy of leaf development. Namely, to address how aberrant cell enlargement is induced and how cell expansion system responds to the inductive condition during compensation, he planned to combine mutants which have a specific defect in each process. However, in many reports about dwarf mutants, histological analysis revealing number and size of cells within the leaves has been insufficient. Thus, the primary defect(s) contributing to changes in organ size in these dwarf mutants remained unclear. Therefore, he analyzed the cell number and size within leaves in several known dwarf mutants. As a result, unexpectedly, most of the well-known dwarf mutants had detects in both cell proliferation and cell expansion and they were wrongly reported from very limited, fragmental observations. Thus, he found that it is necessary to newly isolate cell-number or -size specific mutants to analyze the induction and response processes of compensation. From a large collection of leaf-size mutants established in the laboratory he belongs, he successfully isolated several mutant lines with a spectfic defect in leaf cell number or size. <br />       Then, he utilized these mutants to analyze the induction or response process of compensation. In the analysis of \"induction\" process of compensation, he selected six lines of utants from the above-mentioned mutants isolated, named otigocellula (oli), which had a specific decrease in cell number. Although the induction of compensation is thought to be closely linked to a decrease in cell number, oli mutants did not exhibit compensation. Thus, he thought that the induction of compensation requires not only a decrease in cell number but also some special conditions. But before this study, nothing was known for the condition required for induction of compensation. To clarify conditions, he produced double mutants among oli mutants in which the extent of decrease in cell number is variable. As a result, when the leaf cell number in oli double mutant was significantly decreased than each parental single oli mutant, the leaf cell size was strongly increased. This result indicates a possibillity that the induction of oompensation depends on a decrease in cell number in a threshold-dependent manner. <br />           To further address whether a further decrease in cell number affects cetl size, next, he constructed double mutants between the an3 and the oli mutants. As a result, most of oli an3 double mutants had much fewer and significantly Darger leaf cells than the an3. Exceptionally, oli1 an3 double mutant had a similar number and size of leaf cells to an3. These results indicated that the further decrease in cell number induces an additional and proportional cell enlargement, when cell number fall below a threshold level. It also revealed that the OLI1 and AN3 genes have a function in cell proliferation in the same genetic pathway. <br />           Some researchers have regarded compensation as a result of uncoupling of cell growth and cell division from cell growth. If compensation results from an uncoupling of celf growth and cell division, cell size should be larger in proportion to any decreases in cell number. However, identification of threshold ruled out this possibillty. These findings demonstrate that compensation is not a mere uncoupling of cell cycling and cell enlargement and suggest the existence of yet unknown genetic network between cell proliferation and cell expansion in leaf organogenesis. <br />       For the analysis of \"responsei\" process of compensation, he isolated and utilized ten lines of mutant, that he named extra-small sisters (xs), which have a specific defect in cell expansion but have normal cell numbers in leaves. In the xs single mutants, the palisade cell sizes in mature leaves are about 20 to 50% smaller than wild-type cells. Then, he produced double mutants between xs mutants and an3 to genetically dissect the cell expansion system(s) bunderiying compensation in the an3 mutant. As a result, phenotypes of the palisade cell sizes in all combinations of xs an3 double mutants fall into three classes. In the first class, the compensation was significantly suppressed. Conversely, in the second class, the defective cell expansion conferred by the xs mutations was significantly suppressed by the an3 mutation, and the cell sizes were close to that in the an3 single mutant. The residuafi xs mutations had effects additive to those of the an3 mutation on cell expansion. The endopolyploidy levels in the first class of mutants were decreased, unaffected, or increased, as compared to those in wild type, suggesting that the abnormally enhanced cell expansion observed in an3 is mediated, at least in part, by ploidy-independent mechanisms. Altogether, these results suggest that a defect in cell proliferation in leaf primordia enhances a part of the cell expansion system required for normal cell expansion. <br />      Taken all together, the present study has revealed important clues of leaf size control: the induction process of compensation deponds on a decrease in cete number in a threshold-dependent manner; the response process of oompensation depends on a specific enhancement of normal processes of cell expansion control; and component of genetic networks for the control of leaf cell proliferation and celt expansion. ","subitem_description_type":"Other"}]},"item_1_description_7":{"attribute_name":"学位記番号","attribute_value_mlt":[{"subitem_description":"総研大甲第1068号","subitem_description_type":"Other"}]},"item_1_select_14":{"attribute_name":"所蔵","attribute_value_mlt":[{"subitem_select_item":"有"}]},"item_1_select_8":{"attribute_name":"研究科","attribute_value_mlt":[{"subitem_select_item":"生命科学研究科"}]},"item_1_select_9":{"attribute_name":"専攻","attribute_value_mlt":[{"subitem_select_item":"19 基礎生物学専攻"}]},"item_1_text_10":{"attribute_name":"学位授与年度","attribute_value_mlt":[{"subitem_text_value":"2006"}]},"item_creator":{"attribute_name":"著者","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{"creatorName":"FUJIKURA, Ushio","creatorNameLang":"en"}],"nameIdentifiers":[{}]}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2016-02-17"}],"displaytype":"simple","filename":"甲1068_要旨.pdf","filesize":[{"value":"388.1 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"要旨・審査要旨","url":"https://ir.soken.ac.jp/record/1058/files/甲1068_要旨.pdf"},"version_id":"83c54108-4723-4c3b-9ae5-e6b24906f34f"},{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2016-02-17"}],"displaytype":"simple","filename":"甲1068_本文.pdf","filesize":[{"value":"14.9 MB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"本文","url":"https://ir.soken.ac.jp/record/1058/files/甲1068_本文.pdf"},"version_id":"6a71bba4-f03d-480a-9baa-e00586495ec9"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"eng"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"thesis","resourceuri":"http://purl.org/coar/resource_type/c_46ec"}]},"item_title":"Genetic Analyses of Mechanisms of Compensation in Leaf Organogenesis","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"Genetic Analyses of Mechanisms of Compensation in Leaf Organogenesis"},{"subitem_title":"Genetic Analyses of Mechanisms of Compensation in Leaf Organogenesis","subitem_title_language":"en"}]},"item_type_id":"1","owner":"1","path":["21"],"pubdate":{"attribute_name":"公開日","attribute_value":"2010-02-22"},"publish_date":"2010-02-22","publish_status":"0","recid":"1058","relation_version_is_last":true,"title":["Genetic Analyses of Mechanisms of Compensation in Leaf Organogenesis"],"weko_creator_id":"1","weko_shared_id":1},"updated":"2023-06-20T15:55:54.340287+00:00"}