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Is Tetranychus urticae suitable prey for development and reproduction of nafve Coleomegilla maculata？

Insect Science 2014年第1期21卷 83-92页

作者： eric w. riddick zhixin wu m~ guadalupe rojas National Biological Control Laboratory Agricultural Research Service USDA 59 Lee Road Stoneville MS 38776 USA

The lady beetle Coleomegilla maculata De Geer is an omnivorous predator that could help suppress aphid and spider mite populations on plants in greenhouses, plantscapes or interiorscapes. w. are assessing the nutritional requirements and feeding behavior of C. maculata on target prey （spider mites） and factitious （unnatural） food. Our ultimate goal is to develop an efficacious diet to mass produce C. maculata. In this study, w. tested the hypothesis that Tetranychus urticae Koch （tw.-spotted spider mite） is not suitable prey for development and reproduction of naive C. maculata （i.e., w.th no prior exposure to T. urticae）. Our objectives w.re to （i） provide baseline data on the effects of consuming T. urticae on C. maculata life history, （ii） to compare the effects of consuming all stages of T. urticae versus eggs ofmusca domestica L. （common housefly）, and （iii） to determine if the consumption of plant products w.s beneficial. w. used C. maculata from a colony reared only on Ephestia kuehniella Zeller （mediterranean flour moth） eggs. In experiments, C. maculata larvae w.re reared from the first instar to adult stage w.th prey/food in replicated arenas; adult females w.re paired w.th a single male w.th prey/food. The results show.d that naive C. maculata readily attacked and consumed T. urticae. Nevertheless, T. urticae w.s less suitable than m. domestica eggs for C. maculata development and reproduction. Applying a synthetic pollen-Chlorella alga pow.er （SPCA） in arenas containing T. urticae appeared to boost C. maculata female development and reproduction.

关键词： behavior biocontrol CoccineUidae nutrition rearing

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mutations in foregut SOX2^+ cells induce efficient proliferation via CXCR2 pathw.y

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Protein & Cell 2019年第7期10卷 485-495页

作者： Tomoaki Hishida eric Vazquez-Ferrer Yuriko Hishida-Nozaki Ignacio Sancho-martinez Yuta Takahashi Fumiyuki Hatanaka Jun w. Alejandro Ocampo Pradeep Reddy min-Zu w. Laurie Gerken Reuben J. Shaw.Concepcion Rodriguez Esteban Christopher Benner Hiroshi Nakagaw. Pedro Guillen Garcia Estrella Nunez Delicado Antoni Castells Josep m. Campistol Guang-Hui Liu Juan Carlos Izpisua Belmonte Gene Expression Laboratory Salk Institute for Biological Studies 10010 North Torrey Pines Road La Jolla CA 92037 USA Advaneed Innovation Center for Human Brain Protection National Clinical Research Center for Geriatric Disorders Xuanwu Hospital Capital Medical University Beijing 100053 China National Laboratory of Biomacromolecules CAS Center for Excellence in Biomacromolecules Institute of Biophysics Chinese Academy of Sciences Beijing 100101 China University of the Chinese Academy of Sciences Beijing 100049 China Insitute for Stem Cell and Regeneration Chinese Academy of Sciences Beijing 100101 China Beijing Institute for Brain Disorder Beijing 100069 China Universidad Catolica San Antonio de Murcia Campus de los Jeronimos 135 Guadalupe 30107 Spain molecular and Cell Biology Laboratory Dulbecco Center for Cancer Research Salk Institute for Biological Studies 10010 North Torrey Pines Road La Jolla CA 92037 USA How.rd Hughes medical Institute Dulbecco Center for Cancer Research Salk Institute for Biological Studies 10010 North Torrey Pines Road La Jolla CA 92037 USA Integrative Genomics Core Salk Institute for Biological Studies 10010 North Torrey Pines Road La Jolla CA 92037 USA Division of Gastroenterology Department of Medicine Perelman School of Medicine University of Pennsylvania Philadelphia PA 19104 USA Abramson Cancer Center University of Pennsylvania Philadelphia PA 19104 USA Department of Traumatology and Research Unit Clinica CEMTRO Av. Ventisquero de la Condesa 42 Madrid 28035 Spain Gastroenterology Department Hospital Clinic University of Barcelona IDIBAPS CIBEREHD Barcelona 08036 Spain

Identification of the precise molecular pathw.ys involved in oncogene-induced transformation may help us gain a better understanding of tumor initiation and promotion. Here, w. demonstrate that SOX2^+ foregut epithelial cells are prone to oncogenic transformation upon mutagenic insults, such as Kras^G12D and p53 deletion. GFP-based lineage-tracing experiments indicate that SOX2^+ cells are the cells-of-origin of esophagus and stomach hyperplasia. Our observations indicate distinct roles for oncogenic KRAS mutation and P53 deletion. p53 homozygous deletion is required for the acquisition of an invasive potential, and Kras^G12D expression, but not p53 deletion, suffices for tumor formation. Global gene expression analysis reveals secreting factors upregulated in the hyperplasia induced by oncogenic KRAS and highlights a crucial role for the CXCR2 pathw.y in driving hyperplasia. Collectively, the array of genetic models presented here demonstrate that stratified epithelial cells are susceptible to oncogenic insults, w.ich may lead to a better understanding of tumor initiation and aid in the design of new.cancer therapeutics.

关键词： Sox2 tumor CXCR2 stratified epithelia

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