Chagas Disease

Despite being described for the first time more than 110 years ago, Chagas disease (caused by the parasite Trypanosoma cruzi) persists as one of the most neglected tropical diseases. This persistent neglect of those affected by this disease is evidenced by the ongoing scientific evidence gaps, the difficulty of incorporating new diagnostic and treatment technologies into the market, and public health failures to ensure timely access to diagnosis and treatment associated with the development of consistent surveillance and control actions. As a result, there is a high burden of morbidity and mortality, and poor quality of life, poverty, stigma, and a fear of death persist for affected people, both in endemic areas in Latin America, and in non-endemic areas. This book spans a variety of disciplines and contributes significantly to reducing the gap in scientific knowledge on Chagas disease, towards achieving the Sustainable Development Goals by 2030

Psr1p interacts with SUN/sad1p and EB1/mal3p to establish the bipolar spindle

Regular Abstracts - Sunday Poster Presentations: no. 382During mitosis, interpolar microtubules from two spindle pole bodies (SPBs) interdigitate to create an antiparallel microtubule array for accommodating numerous regulatory proteins. Among these proteins, the kinesin-5 cut7p/Eg5 is the key player responsible for sliding apart antiparallel microtubules and thus helps in establishing the bipolar spindle. At the onset of mitosis, two SPBs are adjacent to one another with most microtubules running nearly parallel toward the nuclear envelope, creating an unfavorable microtubule configuration for the kinesin-5 kinesins. Therefore, how the cell organizes the antiparallel microtubule array in the first place at mitotic onset remains enigmatic. Here, we show that a novel protein psrp1p localizes to the SPB and plays a key role in organizing the antiparallel microtubule array. The absence of psr1+ leads to a transient monopolar spindle and massive chromosome loss. Further functional characterization demonstrates that psr1p is recruited to the SPB through interaction with the conserved SUN protein sad1p and that psr1p physically interacts with the conserved microtubule plus tip protein mal3p/EB1. These results suggest a model that psr1p serves as a linking protein between sad1p/SUN and mal3p/EB1 to allow microtubule plus ends to be coupled to the SPBs for organization of an antiparallel microtubule array. Thus, we conclude that psr1p is involved in organizing the antiparallel microtubule array in the first place at mitosis onset by interaction with SUN/sad1p and EB1/mal3p, thereby establishing the bipolar spindle.postprin

Microscopy Conference 2017 (MC 2017) - Proceedings

Das Dokument enthält die Kurzfassungen der Beiträge aller Teilnehmer an der Mikroskopiekonferenz "MC 2017", die vom 21. bis 25.08.2017, in Lausanne stattfand

Emerg Infect Dis

Emerging Infectious Diseases is providing access to these abstracts on behalf of the ICEID 2022 program committee (http://www.iceid.org), which performed peer review. ICEID is organized by the Centers for Disease Control and Prevention and Task Force for Global Health, Inc.Emerging Infectious Diseases has not edited or proofread these materials and is not responsible for inaccuracies or omissions. All information is subject to change. Comments and corrections should be brought to the attention of the authors.Suggested citation: Authors. Title [abstract]. International Conference on Emerging Infectious Diseases 2022 poster and oral presentation abstracts. Emerg Infect Dis. 2022 Sep [date cited]. http://www.cdc.gov/EID/pdfs/ICEID2022.pdf2022PMC94238981187