Journal articles: 'Buba'

1

Elia, Nada. ""Kum Buba Yali Kum Buba Tambe, Ameen, Ameen, Ameen": Did Some Flying Africans Bow to Allah?" Callaloo 26, no. 1 (2003): 182–202. http://dx.doi.org/10.1353/cal.2003.0009.

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YUE, ZHENFANG. "Leadership Styles of School Leaders and the Mental Health of Teachers in a university in Beijing, China." Pacific International Journal 6, no. 4 (January 1, 2024): 98–102. http://dx.doi.org/10.55014/pij.v6i4.483.

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This study explores the relationship between leadership styles exhibited by school leaders at Beijing University for Business Administration (BUBA) and the mental health of its teaching staff. BUBA, founded in 1994, has been dedicated to providing quality education for over 20 years and has received recognition and support from various sectors. The importance of teacher mental health in the teaching profession is emphasized, as teachers play a multifaceted role beyond imparting knowledge, impacting student outcomes and the overall quality of education. Teacher well-being is closely linked to student learning, and recognizing the mental health challenges teachers face is vital to prevent negative consequences for both educators and students. The research problem seeks to understand the relationship between leadership styles at BUBA and teacher mental health, with objectives that include examining leadership styles, assessing teacher mental health, investigating correlations, identifying contributing factors, and providing recommendations. The research methodology employs a qualitative approach, involving interviews with 10 teachers, to gain in-depth insights. The research findings reveal a diverse range of leadership styles at BUBA, impacting teacher mental health. Collaborative and supportive leadership styles are associated with positive teacher mental health, fostering a conducive work environment. Authoritarian and directive styles, on the other hand, contribute to stress and dissatisfaction among teachers. Factors within leadership styles, such as professional development and recognition, further influence teacher well-being. Recommendations include leadership development, transparent communication channels, and strategies to reduce workload pressures and promote well-being.

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Kotz, Hans-Helmut. "À Francfort : quoi de neuf à la Buba ?" Revue d'économie financière 17, no. 2 (1991): 202–6. http://dx.doi.org/10.3406/ecofi.1991.1727.

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Kotz, Hans-Helmut. "La Buba : à la recherche de l'argent perdu." Revue d'économie financière 29, no. 2 (1994): 331–38. http://dx.doi.org/10.3406/ecofi.1994.2062.

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5

Sheehan, George. "Huba Buba: Not for the Young and Light." Physician and Sportsmedicine 18, no. 3 (March 1990): 21. http://dx.doi.org/10.1080/00913847.1990.11709985.

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Kotz, Hans-Helmut. "À Francfort : la Buba vote pour le « noyau dur »." Revue d'économie financière 22, no. 3 (1992): 226–31. http://dx.doi.org/10.3406/ecofi.1992.1882.

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Wiegandt, Claus-C. "Buba, Hanspeter, Grötzbach, Jochen und Rolf Monheim: Nachhaltige Mobilitätskultur." Geographische Zeitschrift 100, no. 4 (2012): 247–48. http://dx.doi.org/10.25162/gz-2012-0025.

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Lamido, Ibrahim, and Bashir Garba. "Makaɗan Hausa A Gombe: Tasirin Makaɗan Fada A Masarautar Buba Yero." Tasambo Journal of Language, Literature, and Culture 2, no. 01 (May 15, 2023): 138–44. http://dx.doi.org/10.36349/tjllc.2023.v02i01.017.

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Hausawa mutane ne da aka san su da shiga lungu-lungu da saƙo-saƙo na yankunan maƙwabtansu na kusa da na nesa. Mutane ne da ke da sha’awar tafiye-tafiye don neman kyakkyawar matsuguni na samun ɗan abin tasarrufi na sa wa a bakin salati. A duk inda suka ya da zango sukan yi wa al’ummar da suka taras tasiri da harshensu da al’adunsu. Wannan takarda ta yi nazarin makaɗa da mawaƙan fada waɗanda suka kwararo jihar Gombe kuma suke rayuwa suna nishaxantar da masarautar ta Fulani da kaɗe-kadensu da waƙoƙinsu na fasaha da bushe-bushensu. An kuma kawo dalilai da suka haifar da zuwan Huasawa ƙasar Gombe da sabubban cuɗanyarsu da Fulani a Gombe. Takardar ta yi amfani da hanyar hira da masu ba da bayanai da kuma ajiyayyun takardu don tattara bayanai da suka taimaka wajen taskace nau’o’in makaɗa da mawaƙan Hausa da suke masarautar. Daga ciki, an kawo makaɗan taushi da na turu da na kotso da na ganga da na ruwa da kuma masu bushe-bushe. An yi bayanin waɗanda suka assasa kowane kiɗa a masarautar da inda suka fito da waɗanda suka gaje su, da kuma lokutan da suka fi gabatar da waƙoƙin nasu. Binciken ya gano akwai makaɗan Hausa maza da mata a fadar masarautar da suka shafi dukkan rukuni na mawaƙan da aka gabatar a nan sama. An kuma kawo ‘yan misalai na wasu ɗiyan waƙoƙin makaɗan. Binciken ya nuna yadda ‘ya’ya da jikoki da aka haifa a masarautar suka taimaka wajen gina al’ummar nan da aka fi sani da Hausa/Fulani wato narkewar al’adun al’ummu guda biyu waje ɗaya.

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Wang, Shunan, Xinyu Liu, Meng Yang, Dongqi Yuan, Kui Ye, Xin Qu, and Xinchao Wang. "BUBs Are New Biomarkers of Promoting Tumorigenesis and Affecting Prognosis in Breast Cancer." Disease Markers 2022 (April 21, 2022): 1–21. http://dx.doi.org/10.1155/2022/2760432.

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Background. A tumor occurs because of abnormal cell multiplication caused by many variables like a significant disturbance in the regulation of cell growth and the instability of chromosome mitosis. Budding uninhibited by benzimidazoles 1 (BUB1), BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B), and budding uninhibited by benzimidazoles 3 (BUB3) are key regulators of mitosis, and their abnormal expression is highly correlated with breast cancer (BrCa), sarcoma, hepatic carcinoma, and other malignant tumors. However, the occurrence of BUBs (BUB1, BUB1B, and BUB3) and the development of BrCa have not been systematically explained. Methods. Find out the target gene by looking up literature on PubMed and CNKI. Using the R software, TCGA, GEO, Kaplan-Meier Plotter, TIMER, and other databases, we studied the level of transcription, genetic changes, and physiological functions of BUBs in BrCa patients and their relationship with the origin, development, prognosis, immunity, and drug resistance of BrCa patients. Findings. We found that the high expression level of BUBs in BrCa tissues proposed a poor prognosis. The multivariate Cox regression analysis suggested that BUB1B and BUB3 might be independent prognostic factors of BrCa. In addition, the Metascape functional enrichment analysis showed that BUBs may be involved in the composition of the spindle, chromosome, and other structures and play a role in mitosis, sister chromatid separation, and other processes. Pathway enrichment suggests that BUBs may affect the cell cycle and lead to abnormal proliferation. Meanwhile, we also found that BUB3 can negatively regulate B lymphocytes, and BUB1 and BUB1B inhibit immune responses by promoting the secretion level of checkpoint molecules of the immune system, leading to immune escape of tumor cells. Conclusion. We speculate that BUB1, BUB1B, and BUB3 may be therapeutic targets for BrCa patients and also provide new therapeutic strategies for BrCa treatment.

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10

Lewis, E. "Media and Public History: Buba, Voices from a Steeltown Riggs, Ethnic Notions." Oral History Review 16, no. 2 (September 1, 1988): 128–30. http://dx.doi.org/10.1093/ohr/16.2.128.

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11

Novaković, Boris. "Influence of hydraulic pressure on morphometric variability of riffle beetle Elmis maugetii Latreille, 1802 (Coleoptera: Elmidae)." Tehnika 75, no. 1 (2020): 105–9. http://dx.doi.org/10.5937/tehnika2001105n.

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12

Roberts, B. T., K. A. Farr, and M. A. Hoyt. "The Saccharomyces cerevisiae checkpoint gene BUB1 encodes a novel protein kinase." Molecular and Cellular Biology 14, no. 12 (December 1994): 8282–91. http://dx.doi.org/10.1128/mcb.14.12.8282-8291.1994.

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Normal cell multiplication requires that the events of mitosis occur in a carefully ordered fashion. Cells employ checkpoints to prevent cycle progression until some prerequisite step has been completed. To explore the mechanisms of checkpoint enforcement, we previously screened for mutants of Saccharomyces cerevisiae which are unable to recover from a transient treatment with a benzimidazole-related microtubule inhibitor because they fail to inhibit subsequent cell cycle steps. Two of the identified genes, BUB2 and BUB3, have been cloned and described (M. A. Hoyt, L. Totis, and B. T. Roberts, Cell 66:507-517, 1991). Here we present the characterization of the BUB1 gene and its product. Genetic evidence was obtained suggesting that Bub1 and Bub3 are mutually dependent for function, and immunoprecipitation experiments demonstrated a physical association between the two. Sequence analysis of BUB1 revealed a domain with similarity to protein kinases. In vitro experiments confirmed that Bub1 possesses kinase activity; Bub1 was able to autophosphorylate and to catalyze phosphorylation of Bub3. In addition, overproduced Bub1 was found to localize to the cell nucleus.

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Roberts, B. T., K. A. Farr, and M. A. Hoyt. "The Saccharomyces cerevisiae checkpoint gene BUB1 encodes a novel protein kinase." Molecular and Cellular Biology 14, no. 12 (December 1994): 8282–91. http://dx.doi.org/10.1128/mcb.14.12.8282.

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Normal cell multiplication requires that the events of mitosis occur in a carefully ordered fashion. Cells employ checkpoints to prevent cycle progression until some prerequisite step has been completed. To explore the mechanisms of checkpoint enforcement, we previously screened for mutants of Saccharomyces cerevisiae which are unable to recover from a transient treatment with a benzimidazole-related microtubule inhibitor because they fail to inhibit subsequent cell cycle steps. Two of the identified genes, BUB2 and BUB3, have been cloned and described (M. A. Hoyt, L. Totis, and B. T. Roberts, Cell 66:507-517, 1991). Here we present the characterization of the BUB1 gene and its product. Genetic evidence was obtained suggesting that Bub1 and Bub3 are mutually dependent for function, and immunoprecipitation experiments demonstrated a physical association between the two. Sequence analysis of BUB1 revealed a domain with similarity to protein kinases. In vitro experiments confirmed that Bub1 possesses kinase activity; Bub1 was able to autophosphorylate and to catalyze phosphorylation of Bub3. In addition, overproduced Bub1 was found to localize to the cell nucleus.

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14

Zhou, Lu, Hongwei Yang, Zhen Zhang, Yue Liu, Jayantha Epaarachchi, Zhenggang Fang, Liang Fang, Chunhua Lu, and Zhongzi Xu. "Effects of Ligands in Rare Earth Complex on Properties, Functions, and Intelligent Behaviors of Polyurea–Urethane Composites." Polymers 14, no. 10 (May 21, 2022): 2098. http://dx.doi.org/10.3390/polym14102098.

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There is a need to create next-generation polymer composites having high property, unique function, and intelligent behaviors, such as shape memory effect (SME) and self-healing (SH) capability. Rare earth complexes can provide luminescence for polymers, and their dispersion is highly affected by ligand structures. Here, we created three different REOCs with different ligands before studying the effects of ligands on REOC dispersion in polyurea–urethane (PUU) with disulfide bonds in main chains. In addition, the effects of different REOCs on mechanical properties, luminescent functions, and intelligent behaviors of PUU composites were studied. The results showed that REOC I (Sm(TTA)3phen: TTA, thenoyltrifluoroacetone; phen, 1,10-phenanthroline) has incompatible ligands with the PUU matrix. REOC I and REOC III (Sm(BUBA)3phen: BUBA, 4-benzylurea-benzoic acid) with amine and urea groups facilitate their dispersion. It was REOC III that helped the maintenance of mechanical properties of PUU composites due to the good dispersion and the needle-like morphologies. Due to more organic ligands of REOC III, the fluorescence intensity of composite materials is reduced. The shape recovery ratio of the composite was not as good as that of pure PUU when a large amount of fillers was added. Besides, REOC I reduced the self-healing efficiency of PUU composites due to poor dispersion, and the other two REOCs increased the self-healing efficiency. The results showed that ligands in REOCs are important for their dispersion in the PUU matrix. The poor dispersion of REOC I is unbeneficial for mechanical properties and intelligent behavior. The high miscibility of REOC II (Sm(PABA)3phen: PABA, 4-aminobenzoic acid) decreases mechanical properties as well but ensures the good shape recovery ratio and self-healing efficiency. The mediate miscibility and needle-like morphology of REOC III are good for mechanical properties. The shape recovery ratio, however, was decreased.

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Jumbam, Charles Tardzenyuy. "Sabga Lamidate Succession Dispute of 2007: Manipulation and Government Tolerance." East African Scholars Journal of Agriculture and Life Sciences 6, no. 03 (March 19, 2023): 61–71. http://dx.doi.org/10.36349/easjals.2023.v06i03.002.

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This paper presents a succession dispute in the Sabga Lamidate in Cameroon in 2007 between Abdouliy Mamouda and Yerima Adamu Buba, both princes of the Lamidate and argues that the dispute emanated from manipulation by interest groups and the violation of the succession tradition of the Lamidate by government authorities. For about nine decades since creation in 1925, the Sabga Lamidate has experienced a relative and uninterrupted peace until 2007 when this succession dispute provoked uproar and drew attention both from within and without the North West Region of Cameroon. On Monday 20 August 2007, the then Senior Divisional officer (SDO) for Mezam, Jules Marcelline Ndjanga, Alhadji Baba Danpullo and the Lamido of Banyo, Mohaman Gabdo Yaya accompanied by 200 armed mixed gendarmes and police officers, moved into the Sabga Lamidate and performed an enthronement rite placing Abdoulaiy Mamouda as the designatory successor of the late Lamido Adamou Sabga. This action provoked open opposition resulting in a succession dispute in the Lamidate as Adamu Buba, a contender and choice of the people elected democratically by kingmakers and according to tradition was denied the throne. In order to put our facts in a logical order and to ensure the flow of these narratives, we employed a triangulation of both qualitative and quantitative research methodologies, besides knowledge on participatory observation. We also relied more on live video images provided by the MBOSCUDA (Mbororo Social and Cultural Development Association) office in Bamenda including Newspaper reports on the issue at the time. The paper reveals that: The dispute emanated from the determination of Danpullo to grab the Sabga grazing land, The enthronement of Mamouda was contrary to the succession tradition of the Sabga Lamidate and against the will of its kingmakers and their kith and kin; Danpullo and the fon of Kedjom-Ketingo were at the fore front of the manipulation; the Cameroon Government tolerance paved ...

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Tufo, Bereket, and Abdirazak Abdala. "PRE-EXTENSION DEMONSTRATION OF IMPROVED BREAD WHEAT VARIETIES IN DAWRO ZONE AND KONTA SPECIAL WOREDA OF SOUTHERN NATION NATIONALITIES AND PEOPLES REGIONAL STATE, ETHIOPIA." EPH - International Journal of Agriculture and Environmental Research 4, no. 1 (December 27, 2017): 10–14. http://dx.doi.org/10.53555/eijaer.v4i1.27.

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The study was conducted in Dawro Zone of Tocha and Essera Woreda and Konta Special Woreda. The objective of the study was to demonstrate, recommend and transfer the best performing bread wheat varieties based on grain yield performance and farmers’ preference. In each kebele, one FTC and twelve farmers (8 male and four female farmers) were involved during ‘’meher’’ season of the year 2016. Training was given for the selected farmers and other stakeholders. Providing full packages of bread wheat technology- variety Ogolicho, Shorima and local were demonstrated in Konta Special Woreda but variety Shorima, Kakaba and Local were demonstrated in Dawro Zone of Tocha and Essera Woreda. Plot size of 10m X 10m was used and seeds were planted at a rate of 100kg/ha in all fields. The recommended rate of DAP (100kg/ha) and UREA (50 kg/ha) were used. The spacing between plots and row was 1m and 30cm by drilling respectively. Field days were organized; farmers evaluated and selected the best performed varieties depending on their criteria's set. The criteria were earliness, tillering capacity, seed size, spike length, resistance to diseases and grain yield. During farmers’ selection process both female and male farmers had been incorporated so as to avoid gender bias. The result showed that variety Ogolicho was the best yielder with grain yield of 39.7 qt/ha and 36 qt/ha at Buba-damota Kebele and Chaka-bocha Kebele respectively followed by the variety Shorima (37.8 qt/ha at Buba Damota and 29 qt/ha at Chaka-bocha) in Konta Special Woreda. In Tocha and Essera Woreda, variety Shorima was with better grain yield performance at Edget kebele of Tocha Woreda (34.5 qt/ha) and Arsi-bale Kebele of Essera Woreda (34.4 qt/ha) respectively. Therefore, based on the farmers’ criteria and grain yield performance, variety Ogolicho selected as first followed by Shorima in Konta Special Woreda, and variety Shorma in Tocha and Essera Woreda, were recommended with its full packages for further pre-scaling.

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Destra, Edwin, Natasha Anggraeni, Ariel Bagoes Prakoso, Rafidah Hanina Ashil, Jamaludin Jamaludin, and Mika Jaya Juliastina. "SKRINING DAN EDUKASI PENCEGAHAN FRAMBUSIA PUSKESMAS KUPU DI SDN 01 LAWATAN KABUPATEN TEGAL." Jurnal Pengabdian Kepada Masyarakat 2, no. 2 (July 7, 2023): 01–08. http://dx.doi.org/10.54066/abdimas.v2i2.287.

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Frambusia, juga dikenal sebagai purru, patek, pian, buba, atau ambalo, adalah sebuah penyakit tropis yang termasuk dalam kategori Penyakit Tropis yang seringkali Terabaikan (Neglected Tropical Diseases). Diagnosis frambusia dapat dilakukan melalui pemeriksaan klinis dan serologi. Terkadang, ada kasus frambusia tanpa adanya tanda-tanda klinis yang jelas, sehingga beberapa kasus belum terdiagnosis. Penyakit ini disebabkan oleh pola hidup yang kurang menjaga kebersihan dan jika tidak ditangani dengan cepat, dapat menyebabkan komplikasi di masa depan. Pemeriksaan TPHA-RDT dapat digunakan untuk mendeteksi frambusia secara dini. Kegiatan penyuluhan dan deteksi frambusia melibatkan 12 anak sebagai responden. Frambusia umumnya ditemukan pada anak-anak usia dua hingga lima belas tahun. Upaya sosialisasi akan membantu meningkatkan kesadaran masyarakat tentang frambusia dan mengedukasi mereka mengenai tindakan pencegahan yang efektif. Dengan demikian, pengetahuan yang benar tentang frambusia dapat menjadi dasar untuk mengadopsi perilaku pencegahan yang efektif dan menjaga kesehatan individu serta komunitas secara keseluruhan.

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Tasić-Mitić, Ivana. "Estetsko i duhovno uzrastanje dece uz književni tekst - Buba Stojanović, Danijela Mišić: Dečji svetovi u knjigama - mogućnosti tumačenja, Pedagoški fakultet, Vranje, 2018." Zbornik radova Filozofskog fakulteta u Pristini 52, no. 1 (2022): 429–33. http://dx.doi.org/10.5937/zrffp52-34947.

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Shirnekhi, Hazheen K., Jacob A. Herman, Patrick J. Paddison, and Jennifer G. DeLuca. "BuGZ facilitates loading of spindle assembly checkpoint proteins to kinetochores in early mitosis." Journal of Biological Chemistry 295, no. 43 (August 20, 2020): 14666–77. http://dx.doi.org/10.1074/jbc.ra120.013598.

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BuGZ is a kinetochore component that binds to and stabilizes Bub3, a key player in mitotic spindle assembly checkpoint signaling. Bub3 is required for kinetochore recruitment of Bub1 and BubR1, two proteins that have essential and distinct roles in the checkpoint. Both Bub1 and BubR1 localize to kinetochores through interactions with Bub3, which are mediated through conserved GLEBS domains in both Bub1 and BubR1. BuGZ also has a GLEBS domain, which is required for its kinetochore localization as well, presumably mediated through Bub3 binding. Although much is understood about the requirements for Bub1 and BubR1 interaction with Bub3 and kinetochores, much less is known regarding BuGZ's requirements. Here, we used a series of mutants to demonstrate that BuGZ kinetochore localization requires only its core GLEBS domain, which is distinct from the requirements for both Bub1 and BubR1. Furthermore, we found that the kinetics of Bub1, BubR1, and BuGZ loading to kinetochores differ, with BuGZ localizing prior to BubR1 and Bub1. To better understand how complexes containing Bub3 and its binding partners are loaded to kinetochores, we carried out size-exclusion chromatography and analyzed Bub3-containing complexes from cells under different spindle assembly checkpoint signaling conditions. We found that prior to kinetochore formation, Bub3 is complexed with BuGZ but not Bub1 or BubR1. Our results point to a model in which BuGZ stabilizes Bub3 and promotes Bub3 loading onto kinetochores in early mitosis, which, in turn, facilitates Bub1 and BubR1 kinetochore recruitment and spindle assembly checkpoint signaling.

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Wang, Y., and D. J. Burke. "Checkpoint genes required to delay cell division in response to nocodazole respond to impaired kinetochore function in the yeast Saccharomyces cerevisiae." Molecular and Cellular Biology 15, no. 12 (December 1995): 6838–44. http://dx.doi.org/10.1128/mcb.15.12.6838.

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Inhibition of mitosis by antimitotic drugs is thought to occur by destruction of microtubules, causing cells to arrest through the action of one or more mitotic checkpoints. We have patterned experiments in the yeast Saccharomyces cerevisiae after recent studies in mammalian cells that demonstrate the effectiveness of antimitotic drugs at concentrations that maintain spindle structure. We show that low concentrations of nocodazole delay cell division under the control of the previously identified mitotic checkpoint genes BUB1, BUB3, MAD1, and MAD2 and independently of BUB2. The same genes mediate the cell cycle delay induced in ctf13 mutants, limited for an essential kinetochore component. Our data suggest that a low concentration of nocodazole induces a cell cycle delay through checkpoint control that is sensitive to impaired kinetochore function. The BUB2 gene may be part of a separate checkpoint that responds to abnormal spindle structure.

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Taylor, Stephen S., Edward Ha, and Frank McKeon. "The Human Homologue of Bub3 Is Required for Kinetochore Localization of Bub1 and a Mad3/Bub1-related Protein Kinase." Journal of Cell Biology 142, no. 1 (July 13, 1998): 1–11. http://dx.doi.org/10.1083/jcb.142.1.1.

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A feedback control mechanism, or cell cycle checkpoint, delays the onset of anaphase until all the chromosomes are correctly aligned on the mitotic spindle. Previously, we showed that the murine homologue of Bub1 is not only required for checkpoint response to spindle damage, but also restrains progression through a normal mitosis (Taylor, S.S., and F. McKeon. 1997. Cell. 89:727–735). Here, we describe the identification of a human homologue of Bub3, a 37-kD protein with four WD repeats. Like Bub1, Bub3 localizes to kinetochores before chromosome alignment. In addition, Bub3 and Bub1 interact in mammalian cells. Deletion mapping was used to identify the domain of Bub1 required for binding Bub3. Significantly, this same domain is required for kinetochore localization of Bub1, suggesting that the role of Bub3 is to localize Bub1 to the kinetochore, thereby activating the checkpoint in response to unattached kinetochores. The identification of a human Mad3/Bub1-related protein kinase, hBubR1, which can also bind Bub3 in mammalian cells, is described. Ectopically expressed hBubR1 also localizes to kinetochores during prometaphase, but only when hBub3 is overexpressed. We discuss the implications of the common interaction between Bub1 and hBubR1 with hBub3 for checkpoint control.

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Logarinho, Elsa, Tatiana Resende, Cláudia Torres, and Hassan Bousbaa. "The Human Spindle Assembly Checkpoint Protein Bub3 Is Required for the Establishment of Efficient Kinetochore–Microtubule Attachments." Molecular Biology of the Cell 19, no. 4 (April 2008): 1798–813. http://dx.doi.org/10.1091/mbc.e07-07-0633.

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The spindle assembly checkpoint monitors the status of kinetochore–microtubule (K-MT) attachments and delays anaphase onset until full metaphase alignment is achieved. Recently, the role of spindle assembly checkpoint proteins was expanded with the discovery that BubR1 and Bub1 are implicated in the regulation of K-MT attachments. One unsolved question is whether Bub3, known to form cell cycle constitutive complexes with both BubR1 and Bub1, is also required for proper chromosome-to-spindle attachments. Using RNA interference and high-resolution microscopy, we analyzed K-MT interactions in Bub3-depleted cells and compared them to those in Bub1- or BubR1-depleted cells. We found that Bub3 is essential for the establishment of correct K-MT attachments. In contrast to BubR1 depletion, which severely compromises chromosome attachment and alignment, we found Bub3 and Bub1 depletions to produce defective K-MT attachments that, however, still account for significant chromosome congression. After Aurora B inhibition, alignment defects become severer in Bub3- and Bub1-depleted cells, while partially rescued in BubR1-depleted cells, suggesting that Bub3 and Bub1 depletions perturb K-MT attachments distinctly from BubR1. Interestingly, misaligned chromosomes in Bub3- and Bub1-depleted cells were found to be predominantly bound in a side-on configuration. We propose that Bub3 promotes the formation of stable end-on bipolar attachments.

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Aravamudhan, Pavithra, Renjie Chen, Babhrubahan Roy, Janice Sim, and Ajit P. Joglekar. "Dual mechanisms regulate the recruitment of spindle assembly checkpoint proteins to the budding yeast kinetochore." Molecular Biology of the Cell 27, no. 22 (November 7, 2016): 3405–17. http://dx.doi.org/10.1091/mbc.e16-01-0007.

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Recruitment of spindle assembly checkpoint (SAC) proteins by an unattached kinetochore leads to SAC activation. This recruitment is licensed by the Mps1 kinase, which phosphorylates the kinetochore protein Spc105 at one or more of its six MELT repeats. Spc105 then recruits the Bub3-Bub1 and Mad1-Mad2 complexes, which produce the inhibitory signal that arrests cell division. The strength of this signal depends, in part, on the number of Bub3-Bub1 and Mad1-Mad2 molecules that Spc105 recruits. Therefore regulation of this recruitment will influence SAC signaling. To understand this regulation, we established the physiological binding curves that describe the binding of Bub3-Bub1 and Mad1-Mad2 to the budding yeast kinetochore. We find that the binding of both follows the mass action law. Mps1 likely phosphorylates all six MELT repeats of Spc105. However, two mechanisms prevent Spc105 from recruiting six Bub3-Bub1 molecules: low Bub1 abundance and hindrance in the binding of more than one Bub3-Bub1 molecule to the same Spc105. Surprisingly, the kinetochore recruits two Mad1-Mad2 heterotetramers for every Bub3-Bub1 molecule. Finally, at least three MELT repeats per Spc105 are needed for accurate chromosome segregation. These data reveal that kinetochore-intrinsic and -extrinsic mechanisms influence the physiological operation of SAC signaling, potentially to maximize chromosome segregation accuracy.

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Natasia, Novera, Siti Nur Jannah, and MG Isworo Rukmi. "Potensi Antifungi Bakteri Asam Laktat dari Saluran Pencernaan Ayam Kampung terhadap Kapang Aspergillus flavus." Bioma : Berkala Ilmiah Biologi 22, no. 1 (June 27, 2020): 91–102. http://dx.doi.org/10.14710/bioma.22.1.91-102.

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Contamination of Aspergillus flavus can attacks food and feed ingredients, especially seeds during the storage. The using of biological agents, like microbes that have antifungal activity becomes a promising and important solution to be studied. This research aims to find out the antifungal activity of lactic acid bacteria (LAB) from digestive tract of “Kampung” chickens against the growing of A. flavus. Source of the isolates are from colon, ventriculus, and crop. The inoculums of LAB which using were suspension of cell and cell free supernatant (CFS). There were 6 isolates of LAB (Bub1, Bub3, Bub4, V52, C51, and NNB) tested to obtain the potential of antifungal activity, by with well diffusion and and submerged culture method. The results showed that the 5 isolates suspension cell of LAB showed inhibitory zones, except Bub1, whereas all CFS LAB showed the inhibitory zones against the growth of A. flavus in MRSA medium. Furthermore, antifungal activity of LAB against A. flavus to be observed by measuring the dry weight of the mycelium production, as well as the percentage of inhibition during the incubation period. All isolates of LAB, from suspension cell and CFS showing antifungal activity against growth of A. flavus. The Bub3 and NNB isolates, from suspension cell and CFS showed that the best antifungal activity compared to the others.

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Li, Feng, Hyeung Kim, Zhejian Ji, Tianpeng Zhang, Bohong Chen, Yuanlong Ge, Yang Hu, et al. "The BUB3-BUB1 Complex Promotes Telomere DNA Replication." Molecular Cell 70, no. 3 (May 2018): 395–407. http://dx.doi.org/10.1016/j.molcel.2018.03.032.

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Fernandes, Gonçalo. "The first list of Malayalam words at the end of 15th century by a Portuguese seaman." Boletim do Museu Paraense Emílio Goeldi. Ciências Humanas 11, no. 3 (December 2016): 793–809. http://dx.doi.org/10.1590/1981.81222016000300014.

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Abstract MS-804 from the Municipal Library of Porto, Portugal, is a unique copy of the journal of the first voyage to India under Vasco da Gama’s (ca. 1460–1524) command. It describes the voyage subsequent to the departure from the Tagus River, Portugal, on 8 July 1497 until the return up the shallows of the Grande River de Buba, Guinea, on 25 April 1499. The author of the original of this account is probably Álvaro Velho (fl. 1497/1507), born in Barreiro, but the arguments are still weak, being only achieved by deduction. The copyist is also probably John Theotonius, CRSA. The great merit of this document is the fact that the author was a direct eyewitness of all events. In the last appendix, at folio 45, it has a list of 122 useful daily words and expressions in Portuguese and their translation into Malayalam, a provincial Dravidian language spoken in Kerala State, India. It is a relevant testimony of a variety of Malayalam at the end of the 15th century, despite certain transcription mistakes and the scribe’s censorship of some vulgarisms. In this new semi-diplomatic edition, I applied rigorous transcription criteria and corrected earlier editions, adding English translations and Malayalam equivalences.

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Li, Yan, Ludovic Dubreucq, Bruno G. Alvarenga, Matthieu Raynal, and Laurent Bouteiller. "N‐Substituted Benzene‐1‐Urea‐3,5‐Biscarboxamide (BUBA): Easily Accessible C 2 ‐Symmetric Monomers for the Construction of Reversible and Chirally Amplified Helical Assemblies." Chemistry – A European Journal 25, no. 45 (July 8, 2019): 10650–61. http://dx.doi.org/10.1002/chem.201901332.

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Zhang, Qiaoqiao, Hui Zheng, Shengye Yang, Tong Feng, Minwen Jie, Haiyang Chen, and Hao Jiang. "Bub1 and Bub3 regulate metabolic adaptation via macrolipophagy in Drosophila." Cell Reports 42, no. 4 (April 2023): 112343. http://dx.doi.org/10.1016/j.celrep.2023.112343.

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Bokros, Michael, Delaney Sherwin, Marie-Helene Kabbaj, and Yanchang Wang. "Yeast Fin1-PP1 dephosphorylates an Ipl1 substrate, Ndc80, to remove Bub1-Bub3 checkpoint proteins from the kinetochore during anaphase." PLOS Genetics 17, no. 5 (May 25, 2021): e1009592. http://dx.doi.org/10.1371/journal.pgen.1009592.

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The spindle assembly checkpoint (SAC) prevents anaphase onset in response to chromosome attachment defects, and SAC silencing is essential for anaphase onset. Following anaphase onset, activated Cdc14 phosphatase dephosphorylates the substrates of cyclin-dependent kinase to facilitate anaphase progression and mitotic exit. In budding yeast, Cdc14 dephosphorylates Fin1, a regulatory subunit of protein phosphatase 1 (PP1), to enable kinetochore localization of Fin1-PP1. We previously showed that kinetochore-localized Fin1-PP1 promotes the removal of the SAC protein Bub1 from the kinetochore during anaphase. We report here that Fin1-PP1 also promotes kinetochore removal of Bub3, the Bub1 partner, but has no effect on another SAC protein Mad1. Moreover, the kinetochore localization of Bub1-Bub3 during anaphase requires Aurora B/Ipl1 kinase activity. We further showed that Fin1-PP1 facilitates the dephosphorylation of kinetochore protein Ndc80, a known Ipl1 substrate. This dephosphorylation reduces kinetochore association of Bub1-Bub3 during anaphase. In addition, we found that untimely Ndc80 dephosphorylation causes viability loss in response to tensionless chromosome attachments. These results suggest that timely localization of Fin1-PP1 to the kinetochore controls the functional window of SAC and is therefore critical for faithful chromosome segregation.

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Tavormina, Penny A., and Daniel J. Burke. "Cell Cycle Arrest in cdc20 Mutants of Saccharomyces cerevisiae Is Independent of Ndc10p and Kinetochore Function but Requires a Subset of Spindle Checkpoint Genes." Genetics 148, no. 4 (April 1, 1998): 1701–13. http://dx.doi.org/10.1093/genetics/148.4.1701.

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Abstract The spindle checkpoint ensures accurate chromosome segregation by inhibiting anaphase onset in response to altered microtubule function and impaired kinetochore function. In this study, we report that the ability of the anti-microtubule drug nocodazole to inhibit cell cycle progression in Saccharomyces cerevisiae depends on the function of the kinetochore protein encoded by NDC10. We examined the role of the spindle checkpoint in the arrest in cdc20 mutants that arrest prior to anaphase with an aberrant spindle. The arrest in cdc20 defective cells is dependent on the BUB2 checkpoint and independent of the BUB1, BUB3, and MAD spindle checkpoint genes. We show that the lesion recognized by Bub2p is not excess microtubules, and the cdc20 arrest is independent of kinetochore function. We show that Cdc20p is not required for cyclin proteolysis at two points in the cell cycle, suggesting that CDC20 is distinct from genes encoding integral proteins of the anaphase promoting complex.

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Chen, Rey-Huei. "BubR1 is essential for kinetochore localization of other spindle checkpoint proteins and its phosphorylation requires Mad1." Journal of Cell Biology 158, no. 3 (August 5, 2002): 487–96. http://dx.doi.org/10.1083/jcb.200204048.

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The spindle checkpoint delays anaphase onset until all chromosomes have attached properly to the mitotic spindle. Checkpoint signal is generated at kinetochores that are not bound with spindle microtubules or not under tension. Unattached kinetochores associate with several checkpoint proteins, including BubR1, Bub1, Bub3, Mad1, Mad2, and CENP-E. I herein show that BubR1 is important for the spindle checkpoint in Xenopus egg extracts. The protein accumulates and becomes hyperphosphorylated at unattached kinetochores. Immunodepletion of BubR1 greatly reduces kinetochore binding of Bub1, Bub3, Mad1, Mad2, and CENP-E. Loss of BubR1 also impairs the interaction between Mad2, Bub3, and Cdc20, an anaphase activator. These defects are rescued by wild-type, kinase-dead, or a truncated BubR1 that lacks its kinase domain, indicating that the kinase activity of BubR1 is not essential for the spindle checkpoint in egg extracts. Furthermore, localization and hyperphosphorylation of BubR1 at kinetochores are dependent on Bub1 and Mad1, but not Mad2. This paper demonstrates that BubR1 plays an important role in kinetochore association of other spindle checkpoint proteins and that Mad1 facilitates BubR1 hyperphosphorylation at kinetochores.

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Fraschini, Roberta, Elisa Formenti, Giovanna Lucchini, and Simonetta Piatti. "Budding Yeast Bub2 Is Localized at Spindle Pole Bodies and Activates the Mitotic Checkpoint via a Different Pathway from Mad2." Journal of Cell Biology 145, no. 5 (May 31, 1999): 979–91. http://dx.doi.org/10.1083/jcb.145.5.979.

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The mitotic checkpoint blocks cell cycle progression before anaphase in case of mistakes in the alignment of chromosomes on the mitotic spindle. In budding yeast, the Mad1, 2, 3, and Bub1, 2, 3 proteins mediate this arrest. Vertebrate homologues of Mad1, 2, 3, and Bub1, 3 bind to unattached kinetochores and prevent progression through mitosis by inhibiting Cdc20/APC-mediated proteolysis of anaphase inhibitors, like Pds1 and B-type cyclins. We investigated the role of Bub2 in budding yeast mitotic checkpoint. The following observations indicate that Bub2 and Mad1, 2 probably activate the checkpoint via different pathways: (a) unlike the other Mad and Bub proteins, Bub2 localizes at the spindle pole body (SPB) throughout the cell cycle; (b) the effect of concomitant lack of Mad1 or Mad2 and Bub2 is additive, since nocodazole-treated mad1 bub2 and mad2 bub2 double mutants rereplicate DNA more rapidly and efficiently than either single mutant; (c) cell cycle progression of bub2 cells in the presence of nocodazole requires the Cdc26 APC subunit, which, conversely, is not required for mad2 cells in the same conditions. Altogether, our data suggest that activation of the mitotic checkpoint blocks progression through mitosis by independent and partially redundant mechanisms.

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Vernole, Patrizia, Michael H. Neale, Daniela Barcaroli, Eliana Munarriz, Richard Knight, Richard Tomasini, Tak W. Mak, Gerry Melino, and Vincenzo De Laurenzi. "TAp73α binds the kinetochore proteins Bub1 and Bub3 resulting in polyploidy." Cell Cycle 8, no. 3 (February 2009): 421–29. http://dx.doi.org/10.4161/cc.8.3.7623.

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Niikura, Y., H. Ogi, K. Kikuchi, and K. Kitagawa. "BUB3 that dissociates from BUB1 activates caspase-independent mitotic death (CIMD)." Cell Death & Differentiation 17, no. 6 (January 8, 2010): 1011–24. http://dx.doi.org/10.1038/cdd.2009.207.

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Guenette, S., M. Magendantz, and F. Solomon. "Suppression of a conditional mutation in alpha-tubulin by overexpression of two checkpoint genes." Journal of Cell Science 108, no. 3 (March 1, 1995): 1195–204. http://dx.doi.org/10.1242/jcs.108.3.1195.

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To identify proteins that regulate microtubule assembly in Saccharomyces cerevisiae, we screened for multicopy suppressors of a conditional mutation in alpha-tubulin. Cells expressing the recessive allele tub1-729 as their sole alpha-tubulin gene grow normally at permissive temperature. However, at 15 degrees C the cells lose viability and arrest primarily with large buds and quantitatively diminished microtubule structures. Transformation of mutant cells with genomic libraries repeatedly identified three different suppressors: the two wild-type alpha-tubulin genes, TUB1 and TUB3; and BUB3. BUB3 is a checkpoint gene that permits entry into mitosis depending upon the assembly state of microtubules. Excess BUB3 rescues both the loss of viability and microtubule defects but not the benomyl supersensitivity associated with tub1-729. The suppression is specific for the mutation ALA422VAL in TUB1, and does not affect several other mutations in TUB1 that produce the ‘no microtubule’ phenotype. Overexpression of BUB1, which interacts genetically with BUB3 and which is involved in the same checkpoint pathway, also rescues the cold sensitivity of tub1-729, but another checkpoint gene, MAD2, does not. Overexpression of BUB3 in wild-type cells has no detectable growth or microtubule defect, but disruption of the BUB3 gene produces slow growth and benomyl supersensitivity. Our results suggest that BUB1 and BUB3 overexpression modulate an event required for mitotic spindle function which is rate limiting for tub1-729 cells at the restrictive temperature.

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Long, Zeling, Tong Wu, Qunyan Tian, Luke A. Carlson, Wanchun Wang, and Gen Wu. "Expression and prognosis analyses of BUB1, BUB1B and BUB3 in human sarcoma." Aging 13, no. 9 (April 19, 2021): 12395–409. http://dx.doi.org/10.18632/aging.202944.

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Toledo, Chad M., Jacob A. Herman, Jonathan B. Olsen, Yu Ding, Philip Corrin, Emily J. Girard, James M. Olson, Andrew Emili, Jennifer G. DeLuca, and Patrick J. Paddison. "BuGZ Is Required for Bub3 Stability, Bub1 Kinetochore Function, and Chromosome Alignment." Developmental Cell 28, no. 3 (February 2014): 282–94. http://dx.doi.org/10.1016/j.devcel.2013.12.014.

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Krenn, Veronica, Annemarie Wehenkel, Xiaozheng Li, Stefano Santaguida, and Andrea Musacchio. "Structural analysis reveals features of the spindle checkpoint kinase Bub1–kinetochore subunit Knl1 interaction." Journal of Cell Biology 196, no. 4 (February 13, 2012): 451–67. http://dx.doi.org/10.1083/jcb.201110013.

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The function of the essential checkpoint kinases Bub1 and BubR1 requires their recruitment to mitotic kinetochores. Kinetochore recruitment of Bub1 and BubR1 is proposed to rely on the interaction of the tetratricopeptide repeats (TPRs) of Bub1 and BubR1 with two KI motifs in the outer kinetochore protein Knl1. We determined the crystal structure of the Bub1 TPRs in complex with the cognate Knl1 KI motif and compared it with the structure of the equivalent BubR1TPR–KI motif complex. The interaction developed along the convex surface of the TPR assembly. Point mutations on this surface impaired the interaction of Bub1 and BubR1 with Knl1 in vitro and in vivo but did not cause significant displacement of Bub1 and BubR1 from kinetochores. Conversely, a 62-residue segment of Bub1 that includes a binding domain for the checkpoint protein Bub3 and is C terminal to the TPRs was necessary and largely sufficient for kinetochore recruitment of Bub1. These results shed light on the determinants of kinetochore recruitment of Bub1.

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SHMAKOV, ALEKSANDR. "THE ECONOMIC COMPREHENSIONS OF HUMAN BEHAVIOR. HOW TO INFLUENCE THE HUMAN CHOICE? SHOULD YOU LEARN PAINTING IF YOU WANT TO BE A PAINTER? CAN «BUBA» CHANGE ECONOMICS FOR THE BETTER?" Terra Economicus 13, no. 4 (December 2015): 96–131. http://dx.doi.org/10.18522/2073-6606-2015-4-96-131.

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Yang, Yang, Dai Tsuchiya, and Soni Lacefield. "Bub3 promotes Cdc20-dependent activation of the APC/C in S. cerevisiae." Journal of Cell Biology 209, no. 4 (May 18, 2015): 519–27. http://dx.doi.org/10.1083/jcb.201412036.

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The spindle checkpoint ensures accurate chromosome segregation by sending a signal from an unattached kinetochore to inhibit anaphase onset. Numerous studies have described the role of Bub3 in checkpoint activation, but less is known about its functions apart from the spindle checkpoint. In this paper, we demonstrate that Bub3 has an unexpected role promoting metaphase progression in budding yeast. Loss of Bub3 resulted in a metaphase delay that was not a consequence of aneuploidy or the activation of a checkpoint. Instead, bub3Δ cells had impaired binding of the anaphase-promoting complex/cyclosome (APC/C) with its activator Cdc20, and the delay could be rescued by Cdc20 overexpression. Kinetochore localization of Bub3 was required for normal mitotic progression, and Bub3 and Cdc20 colocalized at the kinetochore. Although Bub1 binds Bub3 at the kinetochore, bub1Δ cells did not have compromised APC/C and Cdc20 binding. The results demonstrate that Bub3 has a previously unknown function at the kinetochore in activating APC/C-Cdc20 for normal mitotic progression.

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Mora-Santos, Maria del Mar, America Hervas-Aguilar, Katharina Sewart, Theresa C. Lancaster, John C. Meadows, and Jonathan B. A. Millar. "Bub3-Bub1 Binding to Spc7/KNL1 Toggles the Spindle Checkpoint Switch by Licensing the Interaction of Bub1 with Mad1-Mad2." Current Biology 26, no. 19 (October 2016): 2642–50. http://dx.doi.org/10.1016/j.cub.2016.07.040.

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Sharp-Baker, Hilary, and Rey-Huei Chen. "Spindle Checkpoint Protein Bub1 Is Required for Kinetochore Localization of Mad1, Mad2, Bub3, and Cenp-E, Independently of Its Kinase Activity." Journal of Cell Biology 153, no. 6 (June 11, 2001): 1239–50. http://dx.doi.org/10.1083/jcb.153.6.1239.

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The spindle checkpoint inhibits the metaphase to anaphase transition until all the chromosomes are properly attached to the mitotic spindle. We have isolated a Xenopus homologue of the spindle checkpoint component Bub1, and investigated its role in the spindle checkpoint in Xenopus egg extracts. Antibodies raised against Bub1 recognize a 150-kD phosphoprotein at both interphase and mitosis, but the molecular mass is reduced to 140 upon dephosphorylation in vitro. Bub1 is essential for the establishment and maintenance of the checkpoint and is localized to kinetochores, similar to the spindle checkpoint complex Mad1–Mad2. However, Bub1 differs from Mad1–Mad2 in that Bub1 remains on kinetochores that have attached to microtubules; the protein eventually dissociates from the kinetochore during anaphase. Immunodepletion of Bub1 abolishes the spindle checkpoint and the kinetochore binding of the checkpoint proteins Mad1, Mad2, Bub3, and CENP-E. Interestingly, reintroducing either wild-type or kinase-deficient Bub1 protein restores the checkpoint and the kinetochore localization of these proteins. Our studies demonstrate that Bub1 plays a central role in triggering the spindle checkpoint signal from the kinetochore, and that its kinase activity is not necessary for the spindle checkpoint in Xenopus egg extracts.

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Pangilinan, F., and F. Spencer. "Abnormal kinetochore structure activates the spindle assembly checkpoint in budding yeast." Molecular Biology of the Cell 7, no. 8 (August 1996): 1195–208. http://dx.doi.org/10.1091/mbc.7.8.1195.

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Saccharomyces cerevisiae cells containing one or more abnormal kinetochores delay anaphase entry. The delay can be produced by using centromere DNA mutations present in single-copy or kinetochore protein mutations. This observation is strikingly similar to the preanaphase delay or arrest exhibited in animal cells that experience spontaneous or induced failures in bipolar attachment of one or more chromosomes and may reveal the existence of a conserved surveillance pathway that monitors the state of chromosome attachment to the spindle before anaphase. We find that three genes (MAD2, BUB1, and BUB2) that are required for the spindle assembly checkpoint in budding yeast (defined by antimicrotubule drug-induced arrest or delay) are also required in the establishment and/or maintenance of kinetochore-induced delays. This was tested in strains in which the delays were generated by limited function of a mutant kinetochore protein (ctf13-30) or by the presence of a single-copy centromere DNA mutation (CDEII delta 31). Whereas the MAD2 and BUB1 genes were absolutely required for delay, loss of BUB2 function resulted in a partial delay defect, and we suggest that BUB2 is required for delay maintenance. The inability of mad2-1 and bub1 delta mutants to execute kinetochore-induced delay is correlated with striking increases in chromosome missegregation, indicating that the delay does indeed have a role in chromosome transmission fidelity. Our results also indicated that the yeast RAD9 gene, necessary for DNA damage-induced arrest, had no role in the kinetochore-induced delays. We conclude that abnormal kinetochore structures induce preanaphase delay by activating the same functions that have defined the spindle assembly checkpoint in budding yeast.

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Sodiq, Yushau. "Pragmatism in the Age of Jihad." American Journal of Islam and Society 13, no. 1 (April 1, 1996): 109–12. http://dx.doi.org/10.35632/ajis.v13i1.2338.

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Without doubt, Gomez has made a great contribution to the understandingof Islam in Bundu. Although a few works have been published onIslam in West Africa, Gomez’s work is a valuable addition. The authorbegins by locating Bundu on the map of West Africa and explaining thescope of his research and the sources upon which he relies. Gomez attributesthe success of Bundu as a state to its pragmatic policies, which, healleges, were predetermined by its founders. By pragmatism he means:a policy in which the pursuit of commercial and agriculturaladvantage supersedes all other considerations, to the extent thatalliances and rivalries with both neighboring polities andEuropean powers are determined by economic expediency, andare subject to rapid and frequent realignment. (p. 2)Compliance with this policy implies that the foreign and domesticaffairs are not based on advancing the claims of Islam, but rather on promotingpeaceful coexistence among all groups, be they Muslim or non-Muslim, in Bundu.This book is designed for general readers. The author discusses majorissues in Bundu and Senegambia before the imposition of colonial rule andadministration. He analyzes critically the significant roles played by Almaamis(the imams) Malik Sy, Buba Malik, Maka Jiba, Amadi Gai, BokarSaada, and Mamadu Lamine and provides a clear explanation of the Bundustate’s gradual development from the sixteenth century until 1902. He alsoshows the French administration’s insidious politics of divide and rule in St.Louis, Bakel, and Senegal, which was designed to weaken Bundu by instigatingconflict between one imam and another and to control the trade inthis area (pp. 95-97). Throughout his analysis, Gomez reiterates cautiouslyhis thesis that Bundu’s leaders were never interested in advancing Islam orestablishing a strong Islamic state. Rather, they were “essentially concernedwith preservation and commercial expansion of the state” (p. 99).Toward the end of the book, he deals more with the leadership ofBokar Saada, who reigned for a long time despite the lack of popular support. Bokar Saada was a leader forced on Bundu by French administrators ...

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Hardwick, K. G., and A. W. Murray. "Mad1p, a phosphoprotein component of the spindle assembly checkpoint in budding yeast." Journal of Cell Biology 131, no. 3 (November 1, 1995): 709–20. http://dx.doi.org/10.1083/jcb.131.3.709.

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The spindle assembly checkpoint prevents cells from initiating anaphase until the spindle has been fully assembled. We previously isolated mitotic arrest deficient (mad) mutants that inactivate this checkpoint and thus increase the sensitivity of cells to benomyl, a drug that interferes with mitotic spindle assembly by depolymerizing microtubules. We have cloned the MAD1 gene and show that when it is disrupted yeast cells have the same phenotype as the previously isolated mad1 mutants: they fail to delay the metaphase to anaphase transition in response to microtubule depolymerization. MAD1 is predicted to encode a 90-kD coiled-coil protein. Anti-Mad1p antibodies give a novel punctate nuclear staining pattern and cell fractionation reveals that the bulk of Mad1p is soluble. Mad1p becomes hyperphosphorylated when wild-type cells are arrested in mitosis by benomyl treatment, or by placing a cold sensitive tubulin mutant at the restrictive temperature. This modification does not occur in G1-arrested cells treated with benomyl or in cells arrested in mitosis by defects in the mitotic cyclin proteolysis machinery, suggesting that Mad1p hyperphosphorylation is a step in the activation of the spindle assembly checkpoint. Analysis of Mad1p phosphorylation in other spindle assembly checkpoint mutants reveals that this response to microtubule-disrupting agents is defective in some (mad2, bub1, and bub3) but not all (mad3, bub2) mutant strains. We discuss the possible functions of Mad1p at this cell cycle checkpoint.

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Haruki, Nobuhiro, Hiroko Saito, Tomoko Harano, Shuji Nomoto, Takao Takahashi, Hirotaka Osada, Yoshitaka Fujii, and Takashi Takahashi. "Molecular analysis of the mitotic checkpoint genes BUB1 , BUBR1 and BUB3 in human lung cancers." Cancer Letters 162, no. 2 (January 2001): 201–5. http://dx.doi.org/10.1016/s0304-3835(00)00675-3.

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Windecker, Hanna, Maria Langegger, Stephanie Heinrich, and Silke Hauf. "Bub1 and Bub3 promote the conversion from monopolar to bipolar chromosome attachment independently of shugoshin." EMBO reports 10, no. 9 (August 14, 2009): 1022–28. http://dx.doi.org/10.1038/embor.2009.183.

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Farr, Katie A., and M. Andrew Hoyt. "Bub1p Kinase Activates the Saccharomyces cerevisiae Spindle Assembly Checkpoint." Molecular and Cellular Biology 18, no. 5 (May 1, 1998): 2738–47. http://dx.doi.org/10.1128/mcb.18.5.2738.

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ABSTRACT Saccharomyces cerevisiae BUB1 encodes a protein kinase required for spindle assembly checkpoint function. In the presence of spindle damage, BUB1 is required to prevent cell cycle progression into anaphase. We have identified a dominantly actingBUB1 allele that appears to activate the spindle assembly checkpoint pathway in cells with undamaged spindles. High-level expression of BUB1-5 did not cause detectable spindle damage, yet it delayed yeast cells in mitosis at a stage following bipolar spindle assembly but prior to anaphase spindle elongation. Delayed cells possessed a G2 DNA content and elevated Clb2p mitotic cyclin levels. Unlike cells delayed in mitosis by spindle damage or MPS1 kinase overexpression, hyperphosphorylated forms of the Mad1p checkpoint protein did not accumulate. Similar to cells overexpressing MPS1, the BUB1-5 delay was dependent upon the functions of the other checkpoint genes, includingBUB2 and BUB3 and MAD1,MAD2, and MAD3. We found that the mitotic delay caused by BUB1-5 or MPS1 overexpression was interdependent upon the function of the other. This suggests that the Bub1p and Mps1p kinases act together at an early step in generating the spindle damage signal.

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Loizeau, Sophie. "Bubo bubo." Po&sie 162, no. 4 (2017): 41. http://dx.doi.org/10.3917/poesi.162.0041.

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Abruzzi, Katharine C., Margaret Magendantz, and Frank Solomon. "An α-Tubulin Mutant Demonstrates Distinguishable Functions Among the Spindle Assembly Checkpoint Genes in Saccharomyces cerevisiae." Genetics 161, no. 3 (July 1, 2002): 983–94. http://dx.doi.org/10.1093/genetics/161.3.983.

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Abstract Cells expressing a mutant allele of α-tubulin, tub1-729, are cold sensitive and arrest as large-budded cells with microtubule defects. The cold sensitivity of tub1-729 is suppressed by extra copies of a subset of the mitotic checkpoint genes BUB1, BUB3, and MPS1, but not MAD1, MAD2, and MAD3. This suppression by checkpoint genes does not depend upon their role in the MAD2-dependent spindle assembly checkpoint. In addition, BUB1 requires an intact kinase domain as well as Bub3p to suppress tub1-729. The data suggest that tub1-729 cells are defective in microtubule-kinetochore attachments and that the products of specific checkpoint genes can act either directly or indirectly to affect these attachments.

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Journal articles on the topic 'Buba'

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