Determination of photoreceptor cell fate in the Drosophila retina

1994 ◽  
Vol 4 (1) ◽  
pp. 14-20 ◽  
Author(s):  
Helmut Krämer ◽  
Ross L Cagan
Keyword(s):  
Cell Fate ◽  
Photoreceptor Cell

scholarly journals Specification of cell fate in the developing eye of Drosophila

Development ◽  
1991 ◽  
Vol 113 (Supplement_1) ◽  
pp. 123-130 ◽  
Author(s):  
Ernst Hafen ◽  
Konrad Basler
Keyword(s):  
Tyrosine Kinase ◽  
Cell Fate ◽  
Photoreceptor Cell ◽  
Nuclear Protein ◽  
Single Cells ◽  
Photoreceptor Cells ◽  
Positional Information ◽  
Cellular Interactions ◽  
Eye Imaginal Disc

Determination of cell fate in the developing eye of Drosophila depends on cellular interactions. In the eye imaginal disc, an initially unpatterned epithelial sheath of cells, single cells are specified in regular intervals to become the R8 photoreceptor cells. Genes such as Notch and scabrous participate in this process suggesting that specification of ommatidial founder cells and the formation of bristles in the adult epidermis involve a similar mechanism known as lateral inhibition. The subsequent steps of ommatidial assembly involve a different mechanism: undetermined cells read their position based on the contacts they make with neighbors that have already begun to differentiate. The development of the R7 photoreceptor cell is best understood. The key role seems to be played by sevenless, a receptor tyrosine kinase on the surface of the R7 precursor. It transmits the positional information – most likely encoded by boss on the neighboring R8 cell membrane – into the cell via its tyrosine kinase that activates a signal transduction cascade. Two components of this cascade – Sos and sina – have been identified genetically, sina encodes a nuclear protein whose expression is not limited to R7. Constitutive activation of the sevenless kinase by overexpression results in the diversion of other ommatidial cells into the R7 pathway, suggesting that activation of the sevenless signalling pathway is sufficient to specify R7 development.

STAT3-Mediated Signaling in the Determination of Rod Photoreceptor Cell Fate in Mouse Retina

2004 ◽  
Vol 45 (7) ◽  
pp. 2407 ◽  
Author(s):  
Samuel Shao-Min Zhang ◽  
Jiye Wei ◽  
Hua Qin ◽  
Lixin Zhang ◽  
Bing Xie ◽  
...  
Keyword(s):  
Cell Fate ◽  
Photoreceptor Cell ◽  
Mouse Retina ◽  
Rod Photoreceptor

L3/Lhx8 is involved in the determination of cholinergic or GABAergic cell fate

2005 ◽  
Vol 94 (3) ◽  
pp. 723-730 ◽  
Author(s):  
T. Manabe ◽  
K. Tatsumi ◽  
M. Inoue ◽  
H. Matsuyoshi ◽  
M. Makinodan ◽  
...  
Keyword(s):  
Cell Fate

Involvement of RBP-J in biological functions of mouse Notch1 and its derivatives

Development ◽  
1997 ◽  
Vol 124 (20) ◽  
pp. 4133-4141 ◽  
Author(s):  
H. Kato ◽  
Y. Taniguchi ◽  
H. Kurooka ◽  
S. Minoguchi ◽  
T. Sakai ◽  
...  
Keyword(s):  
Cell Fate ◽  
Mutant Cell ◽  
Precursor Cells ◽  
Physical Interaction ◽  
Binding Motifs ◽  
Cell Lineages ◽  
Transactivation Activity ◽  
Vp16 Fusion ◽  
Myogenic Precursor

Notch is involved in the cell fate determination of many cell lineages. The intracellular region (RAMIC) of Notch1 transactivates genes by interaction with a DNA binding protein RBP-J. We have compared the activities of mouse RAMIC and its derivatives in transactivation and differentiation suppression of myogenic precursor cells. RAMIC comprises two separate domains, IC for transactivation and RAM for RBP-J binding. Although the physical interaction of IC with RBP-J was much weaker than with RAM, transactivation activity of IC was shown to involve RBP-J by using an RBP-J null mutant cell line. IC showed differentiation suppression activity that was generally comparable to its transactivation activity. The RBP-J-VP16 fusion protein, which has strong transactivation activity, also suppressed myogenesis of C2C12. The RAM domain, which has no other activities than binding to RBP-J, synergistically stimulated transactivation activity of IC to the level of RAMIC. The RAM domain was proposed to compete with a putative co-repressor for binding to RBP-J because the RAM domain can also stimulate the activity of RBP-J-VP16. These results taken together, indicate that differentiation suppression of myogenic precursor cells by Notch signalling is due to transactivation of genes carrying RBP-J binding motifs.

scholarly journals Hypoxia in Cell Reprogramming and the Epigenetic Regulations

2021 ◽  
Vol 9 ◽  
Author(s):  
Nariaki Nakamura ◽  
Xiaobing Shi ◽  
Radbod Darabi ◽  
Yong Li
Keyword(s):  
Cell Proliferation ◽  
Cell Fate ◽  
Tissue Regeneration ◽  
Cellular Reprogramming ◽  
Cell Reprogramming ◽  
Cell Renewal ◽  
Cellular Functions ◽  
Stem Cell Renewal ◽  
Epigenetic Regulations

Cellular reprogramming is a fundamental topic in the research of stem cells and molecular biology. It is widely investigated and its understanding is crucial for learning about different aspects of development such as cell proliferation, determination of cell fate and stem cell renewal. Other factors involved during development include hypoxia and epigenetics, which play major roles in the development of tissues and organs. This review will discuss the involvement of hypoxia and epigenetics in the regulation of cellular reprogramming and how interplay between each factor can contribute to different cellular functions as well as tissue regeneration.

Control of photoreceptor cell morphology, planar polarity and epithelial integrity during Drosophila eye development

Development ◽  
2002 ◽  
Vol 129 (9) ◽  
pp. 2247-2258 ◽  
Author(s):  
Amanda T. Pickup ◽  
Michele L. Lamka ◽  
Qi Sun ◽  
Man Lun R. Yip ◽  
Howard D. Lipshitz
Keyword(s):  
Cell Fate ◽  
Cell Morphology ◽  
Photoreceptor Cell ◽  
Zinc Finger Protein ◽  
Photoreceptor Cells ◽  
Planar Polarity ◽  
Tracheal System ◽  
General Role ◽  
Epithelial Integrity ◽  
Jnk Signaling

We report that the hindsight (hnt) gene, which encodes a nuclear zinc-finger protein, regulates cell morphology, cell fate specification, planar cell polarity and epithelial integrity during Drosophila retinal development. In the third instar larval eye imaginal disc, HNT protein expression begins in the morphogenetic furrow and is refined to cells in the developing photoreceptor cell clusters just before their determination as neurons. In hnt mutant larval eye tissue, furrow markers persist abnormally posterior to the furrow, there is a delay in specification of preclusters as cells exit the furrow, there are morphological defects in the preclusters and recruitment of cells into specific R cell fates often does not occur. Additionally, genetically mosaic ommatidia with one or more hnt mutant outer photoreceptor cells, have planar polarity defects that include achirality, reversed chirality and misrotation. Mutants in the JNK pathway act as dominant suppressors of the hnt planar polarity phenotype, suggesting that HNT functions to downregulate JUN kinase (JNK) signaling during the establishment of ommatidial planar polarity. HNT expression continues in the photoreceptor cells of the pupal retina. When an ommatidium contains four or more hnt mutant photoreceptor cells, both genetically mutant and genetically wild-type photoreceptor cells fall out of the retinal epithelium, indicating a role for HNT in maintenance of epithelial integrity. In the late pupal stages, HNT regulates the morphogenesis of rhabdomeres within individual photoreceptor cells and the separation of the rhabdomeres of adjacent photoreceptor cells. Apical F-actin is depleted in hnt mutant photoreceptor cells before the observed defects in cellular morphogenesis and epithelial integrity. The analyses presented here, together with our previous studies in the embryonic amnioserosa and tracheal system, show that HNT has a general role in regulation of the F-actin-based cytoskeleton, JNK signaling, cell morphology and epithelial integrity during development.

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