scholarly journals HairlessPromotes Stable Commitment to the Sensory Organ Precursor Cell Fate by Negatively Regulating the Activity of theNotchSignaling Pathway

1995 ◽  
Vol 172 (2) ◽  
pp. 479-494 ◽  
Author(s):  
Anne G. Bang ◽  
Adina M. Bailey ◽  
James W. Posakony
Keyword(s):  
Cell Fate ◽  
Precursor Cell ◽  
Sensory Organ ◽  
Sensory Organ Precursor

Role of Notch and achaete-scute complex in the expression of Enhancer of split bHLH proteins

Development ◽  
1995 ◽  
Vol 121 (11) ◽  
pp. 3745-3752 ◽  
Author(s):  
V. Jennings ◽  
J. de Celis ◽  
C. Delidakis ◽  
A. Preiss ◽  
S. Bray
Keyword(s):  
Cell Fate ◽  
Notch Pathway ◽  
Interaction Mechanism ◽  
Cell Interaction ◽  
Precursor Cell ◽  
Notch Receptor ◽  
Sensory Organ ◽  
Cell Fate Decisions ◽  
Sensory Organ Precursor ◽  
Enhancer Of Split

The proteins encoded by Notch and the Enhancer of split complex are components of a cell-cell interaction mechanism which is important in many cell fate decisions throughout development. One such decision is the formation of the sensory organ precursor cell during the development of the peripheral nervous system in Drosophila. Cells acquire the potential to be neural through the expression of the proneural genes, and the Notch pathway is required to limit neural fate to a single cell from a proneural cluster. However, despite extensive analysis, the precise pathways linking the proneural with Notch and Enhancer of split gene functions remain obscure. For example, it has been suggested that achaete-scute complex proteins directly activate Enhancer of split genes leaving the action of Notch in the pathway unclear. Using monoclonal antibodies that recognise products of the Enhancer of split complex, we show that these proteins accumulate in the cells surrounding the developing sensory organ precursor cell and that their expression is dependent on the activity of Notch and does not directly correlate with expression of Achaete. We further clarify the pathway by showing that ubiquitous expression of an activated Notch receptor leads to widespread accumulation of Enhancer of split proteins even in the absence of achaete-scute complex proteins. Thus Enhancer of split protein expression in response to Notch activity does not require achaete-scute complex proteins.

Only a subset of the binary cell fate decisions mediated by Numb/Notch signaling in Drosophila sensory organ lineage requires Suppressor of Hairless

Development ◽  
1997 ◽  
Vol 124 (22) ◽  
pp. 4435-4446 ◽  
Author(s):  
S. Wang ◽  
S. Younger-Shepherd ◽  
L.Y. Jan ◽  
Y.N. Jan
Keyword(s):  
Hair Cell ◽  
Cell Fate ◽  
Cell Transformation ◽  
Cell Lineage ◽  
Precursor Cell ◽  
Sensory Organ ◽  
Sheath Cell ◽  
Suppressor Of Hairless ◽  
Asymmetric Divisions ◽  
Sensory Organ Precursor

In Drosophila, an adult external sensory organ (bristle) consists of four distinct cells which arise from a sensory organ precursor cell via two rounds of asymmetric divisions. The sensory organ precursor cell first divides to generate two secondary precursor cells, IIa and IIb. The IIa cell then divides to produce the hair cell and the socket cell. Shortly after, the IIb cell divides to generate the neuron and the sheath cell. The membrane-associated protein Numb has been shown to be required for the first two asymmetric divisions. We now report that a new hypomorphic numb mutant not only displays a double-socket phenotype, due to a hair cell to socket cell transformation, but also a double-sheath phenotype, due to a neuron to sheath cell transformation. This provides direct evidence that numb functions in the neuron/sheath cell lineage as well. Those results, together with our observation from immunofluorescence analysis that Numb forms a crescent in the dividing IIa and IIb cells suggest that asymmetric localization of Numb is important for the cell fate determination in all three asymmetric cell divisions in the sensory organ lineage. Interestingly, we found that in the hair/socket cell lineage but not the neuron/sheath cell lineage, a Suppressor of Hairless mutation acts as a dominant suppressor of numb mutations whereas Hairless mutations act as enhancers of numb. Moreover, epistasis analysis indicates that Suppressor of Hairless acts downstream of numb, and results from in vitro binding analysis suggest that the genetic interaction between numb and Hairless may occur through direct protein-protein interaction. These studies reveal that Suppressor of Hairless is required for only a subset of the asymmetric divisions that depend on the function of numb and Notch.

Hairless is required for the development of adult sensory organ precursor cells in Drosophila

Development ◽  
1991 ◽  
Vol 111 (1) ◽  
pp. 89-104 ◽  
Author(s):  
A.G. Bang ◽  
V. Hartenstein ◽  
J.W. Posakony
Keyword(s):  
Cell Fate ◽  
Spatial Arrangement ◽  
Cell Types ◽  
Precursor Cells ◽  
Precursor Cell ◽  
Sensory Organ ◽  
Specific Cell ◽  
Loss Of Function ◽  
Sensory Organ Precursor ◽  
Mutant Phenotypes

Reduction of the wild-type activity of the gene Hairless (H) results in two major phenotypic effects on the mechanosensory bristles of adult Drosophila. Bristles are either ‘lost’ (i.e. the shaft and socket fail to appear) or they exhibit a ‘double socket’ phenotype, in which the shaft is apparently transformed into a second socket. Analysis of the phenotypes conferred by a series of H mutant genotypes demonstrates (1) that different sensilla exhibit different patterns of response to decreasing levels of H+ function, and (2) that the ‘bristle loss’ phenotype results from greater loss of H+ function than the ‘double socket’ phenotype. The systematic study of H allelic combinations enabled us to identify genotypes that reliably produce specific mutant defects in particular positions on the bodies of adult flies. This permitted us to investigate the cellular development of sensilla in these same positions in larvae and pupae and thereby establish the developmental basis for the mutant phenotypes. We have found that H is required for at least two steps of adult sensillum development. In positions where ‘double socket’ microchaetes appear on the notum of H mutant flies, sensillum precursor cells are present in the developing pupa and divide normally, but their progeny adopt an aberrant spatial arrangement and fail to differentiate correctly. In regions of the notum exhibiting ‘bristle loss’ in adult H mutants, we were unable at the appropriate stages of development to detect sensillum-specific cell types, the precursor cell divisions that generate them, or the primary precursor cells themselves. Thus, the H ‘bristle loss’ phenotype appears to reflect a very early defect in sensillum development, namely the failure to specify and/or execute the sensory organ precursor cell fate. This finding indicates that H is one of a small number of identified genes for which the loss-of-function phenotype is the failure of sensillum precursor cell development.

Two types of asymmetric divisions in the Drosophila sensory organ precursor cell lineage

2000 ◽  
Vol 3 (1) ◽  
pp. 58-67 ◽  
Author(s):  
Fabrice Roegiers ◽  
Susan Younger-Shepherd ◽  
Lily Yeh Jan ◽  
Yuh Nung Jan
Keyword(s):  
Cell Lineage ◽  
Precursor Cell ◽  
Sensory Organ ◽  
Asymmetric Divisions ◽  
Sensory Organ Precursor

scholarly journals Sanpodo controls sensory organ precursor fate by directing Notch trafficking and binding γ-secretase

2013 ◽  
Vol 201 (3) ◽  
pp. 439-448 ◽  
Author(s):  
Alok Upadhyay ◽  
Vasundhara Kandachar ◽  
Diana Zitserman ◽  
Xin Tong ◽  
Fabrice Roegiers
Keyword(s):  
Notch Signaling ◽  
Cell Fate ◽  
Daughter Cell ◽  
Asymmetric Cell Division ◽  
Notch Receptor ◽  
Receptor Internalization ◽  
Sensory Organ ◽  
Cell Fates ◽  
Cellular Context ◽  
Sensory Organ Precursor

In Drosophila peripheral neurogenesis, Notch controls cell fates in sensory organ precursor (SOP) cells. SOPs undergo asymmetric cell division by segregating Numb, which inhibits Notch signaling, into the pIIb daughter cell after cytokinesis. In contrast, in the pIIa daughter cell, Notch is activated and requires Sanpodo, but its mechanism of action has not been elucidated. As Sanpodo is present in both pIIa and pIIb cells, a second role for Sanpodo in regulating Notch signaling in the low-Notch pIIb cell has been proposed. Here we demonstrate that Sanpodo regulates Notch signaling levels in both pIIa and pIIb cells via distinct mechanisms. The interaction of Sanpodo with Presenilin, a component of the γ-secretase complex, was required for Notch activation and pIIa cell fate. In contrast, Sanpodo suppresses Notch signaling in the pIIb cell by driving Notch receptor internalization. Together, these results demonstrate that a single protein can regulate Notch signaling through distinct mechanisms to either promote or suppress signaling depending on the local cellular context.

scholarly journals Van Gogh and Frizzled Act Redundantly in the Drosophila Sensory Organ Precursor Cell to Orient Its Asymmetric Division

PLoS ONE ◽  
2009 ◽  
Vol 4 (2) ◽  
pp. e4485 ◽  
Author(s):  
José-Eduardo Gomes ◽  
Maria Corado ◽  
François Schweisguth
Keyword(s):  
Asymmetric Division ◽  
Precursor Cell ◽  
Sensory Organ ◽  
Van Gogh ◽  
Sensory Organ Precursor
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