CoREST acts as a positive regulator of Notch signaling in the follicle cells ofDrosophila melanogaster

Development ◽  
2012 ◽  
Vol 139 (6) ◽  
pp. e608-e608
Author(s):  
E. Domanitskaya ◽  
T. Schupbach
2011 ◽  
Vol 356 (1) ◽  
pp. 128-129
Author(s):  
Elena Domanitskaya ◽  
Trudi Schupbach

2008 ◽  
Vol 319 (2) ◽  
pp. 527-528
Author(s):  
Yan Yan ◽  
Natalie Denef ◽  
Trudi Schupbach

Development ◽  
2011 ◽  
Vol 138 (9) ◽  
pp. 1737-1745 ◽  
Author(s):  
J. S. Poulton ◽  
Y.-C. Huang ◽  
L. Smith ◽  
J. Sun ◽  
N. Leake ◽  
...  

2011 ◽  
Vol 124 (9) ◽  
pp. e1-e1
Author(s):  
J. S. Poulton ◽  
Y.-C. Huang ◽  
L. Smith ◽  
J. Sun ◽  
N. Leake ◽  
...  

2009 ◽  
Vol 20 (24) ◽  
pp. 5064-5073 ◽  
Author(s):  
Li-Fang Shyu ◽  
Jianjun Sun ◽  
Hui-Min Chung ◽  
Yi-Chun Huang ◽  
Wu-Min Deng

Temporal and spatial regulation of cell division is critical for proper development of multicellular organisms. An important aspect of this regulation is cell-cycle arrest, which in many cell types is coupled with differentiated status. Here we report that the polar cells—a group of follicle cells differentiated early during Drosophila oogenesis—are arrested at G2 phase and can serve as a model cell type for investigation of developmental regulation of cell-cycle arrest. On examining the effects of String, a mitosis-promoting phosphatase Cdc25 homolog, and Notch signaling in polar cells, we found that misexpression of String can trigger mitosis in existing polar cells to induce extra polar cells. Normally, differentiation of the polar cells requires Notch signaling. We found that the Notch-induced extra polar cells arise through recruitment of the neighboring cells rather than promotion of proliferation, and they are also arrested at G2 phase. Notch signaling is probably involved in down-regulating String in polar cells, thus inducing the G2 cell-cycle arrest.


Development ◽  
2017 ◽  
Vol 144 (5) ◽  
pp. 905-915 ◽  
Author(s):  
Jay Prakash Shukla ◽  
Girish Deshpande ◽  
L. S. Shashidhara

Development ◽  
2007 ◽  
Vol 134 (6) ◽  
pp. 1161-1169 ◽  
Author(s):  
E. Assa-Kunik ◽  
I. L. Torres ◽  
E. D. Schejter ◽  
D. S. Johnston ◽  
B.-Z. Shilo

Development ◽  
2002 ◽  
Vol 129 (3) ◽  
pp. 705-717 ◽  
Author(s):  
Jennifer R. McGregor ◽  
Rongwen Xi ◽  
Douglas A. Harrison

Janus kinase (JAK) pathway activity is an integral part of signaling through a variety of ligands and receptors in mammals. The extensive re-utilization and pleiotropy of this pathway in vertebrate development is conserved in other animals as well. In Drosophila melanogaster, JAK signaling has been implicated in embryonic pattern formation, sex determination, larval blood cell development, wing venation, planar polarity in the eye, and formation of other adult structures. Here we describe several roles for JAK signaling in Drosophila oogenesis. The gene for a JAK pathway ligand, unpaired, is expressed specifically in the polar follicle cells, two pairs of somatic cells at the anterior and posterior poles of the developing egg chamber. Consistent with unpaired expression, reduced JAK pathway activity results in the fusion of developing egg chambers. A primary defect of these chambers is the expansion of the polar cell population and concomitant loss of interfollicular stalk cells. These phenotypes are enhanced by reduction of unpaired activity, suggesting that Unpaired is a necessary ligand for the JAK pathway in oogenesis. Mosaic analysis of both JAK pathway transducers, hopscotch and Stat92E, reveals that JAK signaling is specifically required in the somatic follicle cells. Moreover, JAK activity is also necessary for the initial commitment of epithelial follicle cells. Many of these roles are in common with, but distinct from, the known functions of Notch signaling in oogenesis. Consistent with these data is a model in which Notch signaling determines a pool of cells to be competent to adopt stalk or polar fate, while JAK signaling assigns specific identity within that competent pool.


2014 ◽  
Vol 41 (6) ◽  
pp. 317-325 ◽  
Author(s):  
Qinghai Zhang ◽  
Yan Zhang ◽  
Longfei Wu ◽  
Yongfei Yang ◽  
Xue Li ◽  
...  

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