Abstract:
:We use the Dpp morphogen gradient in the Drosophila wing disc as a model to address the fundamental question of how a gradient of a growth factor can produce uniform growth. We first show that proper expression and subcellular localization of components in the Fat tumor-suppressor pathway, which have been argued to depend on Dpp activity differences, are not reliant on the Dpp gradient. We next analyzed cell proliferation in discs with uniformly high Dpp or uniformly low Fat signaling activity and found that these pathways regulate growth in a complementary manner. While the Dpp mediator Brinker inhibits growth in the primordium primarily in the lateral regions, Fat represses growth mostly in the medial region. Together, our results indicate that the activities of both signaling pathways are regulated in a parallel rather than sequential manner and that uniform proliferation is achieved by their complementary action on growth.
journal_name
Dev Celljournal_title
Developmental cellauthors
Schwank G,Tauriello G,Yagi R,Kranz E,Koumoutsakos P,Basler Kdoi
10.1016/j.devcel.2010.11.007subject
Has Abstractpub_date
2011-01-18 00:00:00pages
123-30issue
1eissn
1534-5807issn
1878-1551pii
S1534-5807(10)00534-4journal_volume
20pub_type
杂志文章abstract::Vertebrate ancestors had only cone-like photoreceptors. The duplex retina evolved in jawless vertebrates with the advent of highly photosensitive rod-like photoreceptors. Despite cones being the arbiters of high-resolution color vision, rods emerged as the dominant photoreceptor in mammals during a nocturnal phase ear...
journal_title:Developmental cell
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abstract::Cell competition promotes the elimination of weaker cells from a growing population. Here we investigate how cells of Drosophila wing imaginal discs distinguish "winners" from "losers" during cell competition. Using genomic and functional assays, we have identified several factors implicated in the process, including ...
journal_title:Developmental cell
pub_type: 杂志文章
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journal_title:Developmental cell
pub_type: 杂志文章,评审
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abstract::Endoplasmic reticulum-plasma membrane (ER-PM) junctions are conserved structures defined as regions of the ER that tightly associate with the plasma membrane. However, little is known about the mechanisms that tether these organelles together and why such connections are maintained. Using a quantitative proteomic appr...
journal_title:Developmental cell
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journal_title:Developmental cell
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journal_title:Developmental cell
pub_type: 杂志文章
doi:10.1016/j.devcel.2008.08.008
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journal_title:Developmental cell
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doi:10.1016/j.devcel.2018.04.012
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journal_title:Developmental cell
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journal_title:Developmental cell
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doi:10.1016/j.devcel.2012.03.004
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journal_title:Developmental cell
pub_type: 评论,杂志文章
doi:10.1016/j.devcel.2006.04.017
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journal_title:Developmental cell
pub_type: 杂志文章
doi:10.1016/j.devcel.2017.01.015
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journal_title:Developmental cell
pub_type: 杂志文章
doi:10.1016/j.devcel.2005.11.016
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journal_title:Developmental cell
pub_type: 杂志文章
doi:10.1016/j.devcel.2015.09.016
更新日期:2015-10-26 00:00:00
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journal_title:Developmental cell
pub_type: 杂志文章
doi:10.1016/j.devcel.2019.07.010
更新日期:2019-09-23 00:00:00
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journal_title:Developmental cell
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doi:10.1016/j.devcel.2016.01.005
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doi:10.1016/s1534-5807(03)00323-x
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journal_title:Developmental cell
pub_type: 评论,杂志文章
doi:10.1016/j.devcel.2012.01.021
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journal_title:Developmental cell
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doi:10.1016/j.devcel.2006.08.009
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journal_title:Developmental cell
pub_type: 杂志文章
doi:10.1016/j.devcel.2013.10.024
更新日期:2013-12-09 00:00:00
abstract::Plant steroid hormones, brassinosteroids (BRs), are perceived by a cell surface receptor kinase, BRI1, but how BR binding leads to regulation of gene expression in the nucleus is unknown. Here we describe the identification of BZR1 as a nuclear component of the BR signal transduction pathway. A dominant mutation bzr1-...
journal_title:Developmental cell
pub_type: 杂志文章
doi:10.1016/s1534-5807(02)00153-3
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journal_title:Developmental cell
pub_type: 评论,杂志文章
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journal_title:Developmental cell
pub_type: 杂志文章
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journal_title:Developmental cell
pub_type: 杂志文章
doi:10.1016/s1534-5807(02)00170-3
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