{"_buckets": {"deposit": "af3b9bd1-b901-41a0-8624-5133c31c6025"}, "_deposit": {"created_by": 1, "id": "894", "owners": [1], "pid": {"revision_id": 0, "type": "depid", "value": "894"}, "status": "published"}, "_oai": {"id": "oai:ir.soken.ac.jp:00000894", "sets": ["20"]}, "author_link": ["9854", "9853", "9852"], "item_1_biblio_info_21": {"attribute_name": "書誌情報（ソート用）", "attribute_value_mlt": [{"bibliographicIssueDates": {"bibliographicIssueDate": "1994-03-24", "bibliographicIssueDateType": "Issued"}, "bibliographic_titles": [{}]}]}, "item_1_creator_2": {"attribute_name": "著者名", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "安田, 二朗"}], "nameIdentifiers": [{"nameIdentifier": "9852", "nameIdentifierScheme": "WEKO"}]}]}, "item_1_creator_3": {"attribute_name": "フリガナ", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "ヤスダ, ジロウ"}], "nameIdentifiers": [{"nameIdentifier": "9853", "nameIdentifierScheme": "WEKO"}]}]}, "item_1_date_granted_11": {"attribute_name": "学位授与年月日", "attribute_value_mlt": [{"subitem_dategranted": "1994-03-24"}]}, "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_1": {"attribute_name": "ID", "attribute_value_mlt": [{"subitem_description": "1994024", "subitem_description_type": "Other"}]}, "item_1_description_12": {"attribute_name": "要旨", "attribute_value_mlt": [{"subitem_description": "　　　Roles of viral NS and M proteins on the influenza virus growth were\u003cbr /\u003e examined. The NS proteins of influenza virus, NS1I and NS2, are encoded\u003cbr /\u003e by RNA segment 8. The NSI proitein is encoded by a colinear mRNA\u003cbr /\u003e transcript, whereas thc NS2 protein with the molecular weight of 14.2\u003cbr /\u003e kilodaltons (kDa) is synthesid after splicing of NSI mRNA. Up to now,\u003cbr /\u003e these NS proteins are believed to exist only in virus-infected cells. The NSl\u003cbr /\u003e protein, which localizes in nuclei of virus-infected cells, recognizes the \u003ci\u003ecis\u003c/i\u003e-\u003cbr /\u003eacting sequence on NSI mRNA and controls its splicing to NS2 mRNA.\u003cbr /\u003e NS2 is also present mainly in the nuclei. At present, however, little is\u003cbr /\u003e known on the function of this protein. This study indicates that the NS2\u003cbr /\u003e protein, previously considered as one of the two nonstructural proteins (NS 1\u003cbr /\u003e and NS2), exists in virus particles as a structural component. By\u003cbr /\u003e immunochemical method, the number of NS2 molecules in a virus particle\u003cbr /\u003e was estimated to be 130-200 molecules. After solubilization of viral\u003cbr /\u003e enve]ope, NS2 was still associated with ribonucleoprotein (RNP) cores, but\u003cbr /\u003e was later dissociated from RNP upon removal of the membrane M1 protein.\u003cbr /\u003e A filter-binding assay \u003ci\u003ein vitro\u003c/i\u003e indlicated direct protein-protein contact\u003cbr /\u003e between M1 ancl NS2. Following chemical cleavage of the M1 protein,\u003cbr /\u003e NS2 was found to bincl only a C-terminal fragment of M1. By an\u003cbr /\u003e immunoprecipitation method, NS2-M1 complexes were also detected in\u003cbr /\u003e virus-infected cel] lysates. These observations altogether indicate specific\u003cbr /\u003e molecu]ar nteraction between M1 and NS2, suggestlng that NS2 regulates\u003cbr /\u003e the function of M1 or vice versa. \u003cbr /\u003e　　　The M gene of influenza viruses encodes 2 proteins, M1 and M2.\u003cbr /\u003e The M 1 protein is tightly associated with virions forming a matrix, which\u003cbr /\u003e associates with RNP at its internal surface but interacts with envelope at its\u003cbr /\u003e external surface. M1 interacts with both NP, thereby interferes with the\u003cbr /\u003e function of RNP-associated RNA polymerase, and NS2 in virions. In\u003cbr /\u003e virus-infected cells, M1 is involved in both early (uncoating and import of\u003cbr /\u003e RNP into infectecl nuc]ei) and late (assembly of virions during maturation\u003cbr /\u003e and export of RNP from nuclei into cytoplasm) stages of virus growth. On\u003cbr /\u003e the othcr hand, M2 forms an ion channel and is considered to control the\u003cbr /\u003e transport of hemagglutinin (HA). M2 may also control uncoating step to\u003cbr /\u003e release RNP in the early phase of virus infection. Genetic studies described\u003cbr /\u003e in this report suggested that one or both of the M proteins have a regulatory\u003cbr /\u003e role(s) of the rate of virus growth. Influenza virus A/WSN/33 forms large\u003cbr /\u003e plaques (\u003e3mm diameter) on MDCK cells whereas A/Aichi/2/68 forms\u003cbr /\u003e on]y small plaques (\u003c1mm diameter). Fast growing reassortants (AWM),\u003cbr /\u003e isolated by mixed infection of MDCK cells with these two virus strains in\u003cbr /\u003e the presence of anti-WSN antibodies, all carried the M gene from WSN.\u003cbr /\u003e On MDCK cells, these reassortants produced progeny viruses as rapidly as\u003cbr /\u003e did WSN, and the virus yield was as high as Aichi. Pulse-labeling\u003cbr /\u003e experiments at various times after virus infectlon showed that the reassortant\u003cbr /\u003e AWM started to synthesize viral proteins earlier than Aichi. To determine\u003cbr /\u003e which of the two M proteins, M1 or M2, is responsible for the fast rate of\u003cbr /\u003e virus growth, an attempt was made to make recombinant viruses possessing\u003cbr /\u003e the chimeric M gene between WSN and Aichi. For this purpose, I\u003cbr /\u003e employed a newly developed RNA-transfection method into helper virus-\u003cbr /\u003einfected cells. The ts-mutant derived from WSN, ts5 1 , carrying the ts lesion\u003cbr /\u003e only in thc M gene, were used as a helper virus to rescue the chimeric M\u003cbr /\u003e gene RNA. A transfectant virus carrying a chimeric M gene consisting of\u003cbr /\u003e WSN-MI and Aichi-M2, CWA20, was generated by using an improved\u003cbr /\u003e reverse genetics system. The CWA20 virus formed large-sized plaques,\u003cbr /\u003e indicating that thc M1 protein, but not the M2 protein, was responsible for\u003cbr /\u003e this rapid growth of WSN-type. Taken together, I conclude that the\u003cbr /\u003e reassortant viruses entry into growth cycle faster than the parent Aichi strain,\u003cbr /\u003e presumably due to rapid uncoating of the M1 protein from RNP cores. As a\u003cbr /\u003e result of rapid uncoating, the reassortant RNP should be transported into\u003cbr /\u003e host nuclei faster than Aichi RNP, ultimately leading to an early onset of\u003cbr /\u003e transcription of the viral genes.", "subitem_description_type": "Other"}]}, "item_1_description_18": {"attribute_name": "フォーマット", "attribute_value_mlt": [{"subitem_description": "application/pdf", "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88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": "18 遺伝学専攻"}]}, "item_1_text_10": {"attribute_name": "学位授与年度", "attribute_value_mlt": [{"subitem_text_value": "1993"}]}, "item_1_text_20": {"attribute_name": "業務メモ", "attribute_value_mlt": [{"subitem_text_value": "（2018年2月19日）本籍など個人情報の記載がある旧要旨・審査要旨を個人情報のない新しいものに差し替えた。承諾書等未確認。要確認該当項目修正のこと。"}]}, "item_creator": {"attribute_name": "著者", "attribute_type": "creator", "attribute_value_mlt": [{"creatorNames": [{"creatorName": "YASUDA, Jiro", "creatorNameLang": "en"}], "nameIdentifiers": [{"nameIdentifier": "9854", "nameIdentifierScheme": "WEKO"}]}]}, "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", "download_preview_message": "", "file_order": 0, "filename": "甲88_要旨.pdf", "filesize": [{"value": "284.7 kB"}], "format": "application/pdf", "future_date_message": "", "is_thumbnail": false, "licensetype": "license_11", "mimetype": "application/pdf", "size": 284700.0, "url": {"label": "要旨・審査要旨 / Abstract, Screening Result", "url": "https://ir.soken.ac.jp/record/894/files/甲88_要旨.pdf"}, "version_id": "fb46043a-beea-4713-b2af-deeee2cd2f67"}, {"accessrole": "open_date", "date": [{"dateType": "Available", "dateValue": "2016-02-17"}], "displaytype": "simple", "download_preview_message": "", "file_order": 1, "filename": "甲88_本文.pdf", "filesize": [{"value": "1.8 MB"}], "format": "application/pdf", "future_date_message": "", "is_thumbnail": false, "licensetype": "license_11", "mimetype": "application/pdf", "size": 1800000.0, "url": {"label": "本文", "url": "https://ir.soken.ac.jp/record/894/files/甲88_本文.pdf"}, "version_id": "ee0a8772-d403-42ed-9cc2-8152cfdec2b1"}]}, "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": "インフルエンザウイルスの増殖の制御機構：ウイルス蛋白質の役割", "item_titles": {"attribute_name": "タイトル", "attribute_value_mlt": [{"subitem_title": "インフルエンザウイルスの増殖の制御機構：ウイルス蛋白質の役割"}, {"subitem_title": "Control of growth and assembly of influenza virus: Role of viral proteins", "subitem_title_language": "en"}]}, "item_type_id": "1", "owner": "1", "path": ["20"], "permalink_uri": "https://ir.soken.ac.jp/records/894", "pubdate": {"attribute_name": "公開日", "attribute_value": "2010-02-22"}, "publish_date": "2010-02-22", "publish_status": "0", "recid": "894", "relation": {}, "relation_version_is_last": true, "title": ["インフルエンザウイルスの増殖の制御機構：ウイルス蛋白質の役割"], "weko_shared_id": 1}