The Drosophila T-box transcription factor Midline functions within the Notch–Delta signaling pathway to specify sensory organ precursor cell fates and regulates cell survival within the eye imaginal disc

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.

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Bazooka is required for localization of determinants and controlling proliferation in the sensory organ precursor cell lineage in Drosophila

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.261555598 ◽

2001 ◽

Vol 98 (25) ◽

pp. 14469-14474 ◽

Cited By ~ 27

Author(s):

F. Roegiers ◽

S. Younger-Shepherd ◽

L. Y. Jan ◽

Y. N. Jan

Keyword(s):

Cell Lineage ◽

Precursor Cell ◽

Sensory Organ ◽

Sensory Organ Precursor

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

Nature Cell Biology ◽

10.1038/35050568 ◽

2000 ◽

Vol 3 (1) ◽

pp. 58-67 ◽

Cited By ~ 71

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

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Sibling cell fate in the Drosophila adult external sense organ lineage is specified by prospero function, which is regulated by Numb and Notch

Development ◽

10.1242/dev.126.10.2083 ◽

1999 ◽

Vol 126 (10) ◽

pp. 2083-2092 ◽

Cited By ~ 9

Author(s):

G.V. Reddy ◽

V. Rodrigues

Keyword(s):

Transcription Factor ◽

Notch Signaling ◽

Cell Fate ◽

Sense Organ ◽

Sensory Organ ◽

Sensory Organs ◽

Cell Fates ◽

Homeodomain Transcription Factor ◽

Intrinsic Signal ◽

Sensory Organ Precursors

Specification of cell fate in the adult sensory organs is known to be dependent on intrinsic and extrinsic signals. We show that the homeodomain transcription factor Prospero (Pros) acts as an intrinsic signal for the specification of cell fates within the mechanosensory lineage. The sensory organ precursors divide to give rise to two secondary progenitors - PIIa and PIIb. Pros is expressed in PIIb, which gives rise to the neuron and thecogen cells. Loss of Pros function affects the identity of PIIb and neurons fail to differentiate. Pros misexpression is sufficient for the transformation of PIIa to PIIb fate. The expression of Pros in the normal PIIb cell appears to be regulated by Notch signaling.

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The beta-catenin homolog BAR-1 and LET-60 Ras coordinately regulate the Hox gene lin-39 during Caenorhabditis elegans vulval development

Development ◽

10.1242/dev.125.18.3667 ◽

1998 ◽

Vol 125 (18) ◽

pp. 3667-3680 ◽

Cited By ~ 39

Author(s):

D.M. Eisenmann ◽

J.N. Maloof ◽

J.S. Simske ◽

C. Kenyon ◽

S.K. Kim

Keyword(s):

Signaling Pathway ◽

Cell Fate ◽

Precursor Cell ◽

Ras Signaling ◽

Beta Catenin ◽

Cell Fates ◽

Vulval Development ◽

Hox Gene ◽

C Elegans ◽

Vulval Precursor Cell

In C. elegans, the epithelial Pn.p cells adopt either a vulval precursor cell fate or fuse with the surrounding hypodermis (the F fate). Our results suggest that a Wnt signal transduced through a pathway involving the beta-catenin homolog BAR-1 controls whether P3.p through P8.p adopt the vulval precursor cell fate. In bar-1 mutants, P3.p through P8.p can adopt F fates instead of vulval precursor cell fates. The Wnt/bar-1 signaling pathway acts by regulating the expression of the Hox gene lin-39, since bar-1 is required for LIN-39 expression and forced lin-39 expression rescues the bar-1 mutant phenotype. LIN-39 activity is also regulated by the anchor cell signal/let-23 receptor tyrosine kinase/let-60 Ras signaling pathway. Our genetic and molecular experiments show that the vulval precursor cells can integrate the input from the BAR-1 and LET-60 Ras signaling pathways by coordinately regulating activity of the common target LIN-39 Hox.

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

The Journal of Cell Biology ◽

10.1083/jcb.201209023 ◽

2013 ◽

Vol 201 (3) ◽

pp. 439-448 ◽

Cited By ~ 13

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.

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