The segment polarity gene hedgehog is required for progression of the morphogenetic furrow in the developing Drosophila eye

Ma, Chaoyong; Zhou, Ying; Beachy, Philip A.; Moses, Kevin

doi:10.1016/0092-8674(93)90536-y

Cited by 405 publications

(251 citation statements)

References 54 publications

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“…2D). The reason for this differential effect is unknown; however, it has been shown that initiation of development at the posterior margin is driven by dpp (Wiersdorff et al 1996; Chanut and Heberlein 1997; Pignoni and Zipursky 1997), whereas its internal propagation depends on hh (Heberlein et al 1993(Heberlein et al , 1995Ma et al 1993). Moreover, clones of cells mutant for the Dpp receptor thick veins proliferate significantly only when they include the posterior margin (Burke and Basler 1996).…”

Section: Eyelid Affects Patterning Of the Eye Imaginal Discmentioning

confidence: 99%

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eyelidantagonizes wingless signaling during Drosophiladevelopment and has homology to the Bright family of DNA-binding proteins

Treisman

Luk²,

Rubin³

et al. 1997

Genes Dev.

115

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In Drosophila, pattern formation at multiple stages of embryonic and imaginal development depends on the same intercellular signaling pathways. We have identified a novel gene, eyelid (eld), which is required for embryonic segmentation, development of the notum and wing margin, and photoreceptor differentiation. In these tissues, eld mutations have effects opposite to those caused by wingless (wg) mutations. eld encodes a widely expressed nuclear protein with a region homologous to a novel family of DNA-binding domains. Based on this homology and on the phenotypic analysis, we suggest that Eld could act as a transcription factor antagonistic to the Wg pathway.

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Section: Eyelid Affects Patterning Of the Eye Imaginal Discmentioning

confidence: 99%

“…Progression of the furrow depends on the expression of hh by differentiating photoreceptors located posterior to the MF (Heberlein et al 1993;Ma et al 1993;Heberlein et al 1995). Hh protein induces more anteriorly-located cells to differentiate and themselves express hh, thereby creating a cycle of induction that moves the furrow across the eye disc.…”

mentioning

confidence: 99%

eyelidantagonizes wingless signaling during Drosophiladevelopment and has homology to the Bright family of DNA-binding proteins

Treisman

Luk²,

Rubin³

et al. 1997

Genes Dev.

115

View full text Add to dashboard Cite

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“…The impetus for asking the first question lies in the fact that Hh signaling is also required for furrow initiation (Ma et al, 1993;Heberlein et al, 1993;Chanut and Heberlein, 1995;Heberlein et al, 1995;Ma and Moses, 1995;Pan and Rubin, 1995;Strutt et al, 1995;Wehrli and Tomlinson, 1995). However, expression of emc under the control of either dpp or ey enhancers, both of which drive expression at the posterior margin of the disc (Blackman et al, 1991;Hauck et al, 1999), failed to have any observable effect on furrow initiation (supplementary material Fig.…”

Section: Emc Both Regulates and Cooperates With Wg Signaling To Prevementioning

confidence: 99%

“…Progression of the furrow and dpp activation are both dependent upon Hh signaling (Heberlein et al, 1993;Ma et al, 1993;Heberlein et al, 1995;Domínguez and Hafen, 1997;Borod and Heberlein, 1998). We attempted to ascertain whether furrow acceleration and increased dpp transcription within emc-null clones are due to elevated Hh signaling.…”

Section: Emc Controls the Pace Of Furrow Movement Through Regulation mentioning

confidence: 99%

Extramacrochaetae imposes order on the Drosophila eye by refining the activity of the Hedgehog signaling gradient

Spratford

Kumar

2013

Development

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The compound eye of Drosophila melanogaster is configured by a differentiating wave, the morphogenetic furrow, that sweeps across the eye imaginal disc and transforms thousands of undifferentiated cells into a precisely ordered repetitive array of 800 ommatidia. The initiation of the furrow at the posterior margin of the epithelium and its subsequent movement across the eye field is controlled by the activity of the Hedgehog (Hh) signaling pathway. Differentiating photoreceptors that lie behind the furrow produce and secrete the Hh morphogen, which is captured by cells within the furrow itself. This leads to the stabilization of the full-length form of the zinc-finger transcription factor Cubitus interruptus (Ci155), the main effector of Hh signaling. Ci155 functions as a transcriptional activator of a number of downstream targets, including decapentaplegic (dpp), a TGFβ homolog. In this report, we describe a mechanism that is in place within the fly retina to limit Hh pathway activity within and ahead of the furrow. We demonstrate that the helix-loop-helix (HLH) protein Extramacrochaetae (Emc) regulates Ci155 levels. Loss of emc leads to an increase in Ci155 levels, nuclear migration, apical cell constriction and an acceleration of the furrow. We find that these roles are distinct from the bHLH protein Hairy (H), which we show restricts atonal (ato) expression ahead of the furrow. Secondary furrow initiation along the dorsal and ventral margins is blocked by the activity of the Wingless (Wg) pathway. We also show that Emc regulates and cooperates with Wg signaling to inhibit lateral furrow initiation.

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“…Furthermore, no defects in the positioning of mitochondria or nuclei, were observed. Overall, although the organization of photoreceptor cell cytoplasm was mildly affected by a loss of KHC, ultrastructural changes known to correlate with serious disruptions of the recycling and secretory pathways were not seen.During eye development, cell specification is controlled through cell-cell signaling, which requires membrane proteins and secreted morphogens (Heberlein et al, 1993(Heberlein et al, , 1995Ma et al, 1995) (reviewed by Dickson and Hafen, 1993;Wolff and Ready, 1993). If photoreceptors in Khc null test clones were aberrant or missing as a consequence of poor signaling, the effect should have been nonautonomous: mutant cells could cause defects in neighboring wild-type cells, or wildtype cells could rescue the defects in neighboring mutant cells.…”

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confidence: 99%

Clonal Tests of Conventional Kinesin Function during Cell Proliferation and Differentiation

Brendza

Sheehan

Turner

et al. 2000

MBoC

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Null mutations in the Drosophila Kinesin heavy chain gene (Khc), which are lethal during the second larval instar, have shown that conventional kinesin is critical for fast axonal transport in neurons, but its functions elsewhere are uncertain. To test other tissues, single imaginal cells in young larvae were rendered null for Khc by mitotic recombination. Surprisingly, the null cells produced large clones of adult tissue. The rates of cell proliferation were not reduced, indicating that conventional kinesin is not essential for cell growth or division. This suggests that in undifferentiated cells vesicle transport from the Golgi to either the endoplasmic reticulum or the plasma membrane can proceed at normal rates without conventional kinesin. In adult eye clones produced by null founder cells, there were some defects in differentiation that caused mild ultrastructural changes, but they were not consistent with serious problems in the positioning or transport of endoplasmic reticulum, mitochondria, or vesicles. In contrast, defective cuticle deposition by highly elongated Khc null bristle shafts suggests that conventional kinesin is critical for proper secretory vesicle transport in some cell types, particularly ones that must build and maintain long cytoplasmic extensions. The ubiquity and evolutionary conservation of kinesin heavy chain argue for functions in all cells. We suggest interphase organelle movements away from the cell center are driven by multilayered transport mechanisms; that is, individual organelles can use kinesin-related proteins and myosins, as well as conventional kinesin, to move toward the cell periphery. In this case, other motors can compensate for the loss of conventional kinesin except in cells that have extremely long transport tracks. INTRODUCTIONVesicle transport is important in eukaryotic cells for the addition of material to the plasma membrane, for secretion, and for cell polarity. Active vesicle transport is thought to be driven by mechanochemical enzymes (motor proteins). Motors attach to vesicle membranes and then use ATP hydrolysis to drive unidirectional movement along polar cytoskeletal filaments. Characterized members of the myosin family of motors move toward the barbed or fast-growing ends of actin filaments with the exception of myosin VI, which moves toward the pointed or slow-growing ends (Wells et al., 1999) (reviewed by Sellers and Goodson, 1995). Actin filaments in undifferentiated and in some differentiated cell types are highly concentrated in the cortex (WatermanStorer et al., 1998; reviewed by Cramer, 1999). Cytoplasmic myosins may therefore be important for anchoring or moving vesicles when they are near the plasma membrane (Fath et al., 1994). Motors in the kinesin and dynein families move along microtubules. Characterized dyneins and members of the C-terminal kinesin subfamily move toward microtubule minus ends, whereas other kinesins that act as motors move toward microtubule plus ends (reviewed by Vale and Fletterick, 1997;Hirokawa, 1998;Goldstein and Ya...

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The segment polarity gene hedgehog is required for progression of the morphogenetic furrow in the developing Drosophila eye

Cited by 405 publications

References 54 publications

eyelidantagonizes wingless signaling during Drosophiladevelopment and has homology to the Bright family of DNA-binding proteins

eyelidantagonizes wingless signaling during Drosophiladevelopment and has homology to the Bright family of DNA-binding proteins

Extramacrochaetae imposes order on the Drosophila eye by refining the activity of the Hedgehog signaling gradient

Clonal Tests of Conventional Kinesin Function during Cell Proliferation and Differentiation

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