scholarly journals Control of CNS midline transcription by asymmetric E-box-like elements: similarity to xenobiotic responsive regulation

Development ◽  
1994 ◽  
Vol 120 (12) ◽  
pp. 3563-3569 ◽  
Author(s):  
K.A. Wharton ◽  
R.G. Franks ◽  
Y. Kasai ◽  
S.T. Crews

Central nervous system midline cells constitute a discrete group of Drosophila embryonic cells with numerous functional and developmental roles. Corresponding to their separate identity, the midline cells display patterns of gene expression distinct from the lateral central nervous system. A conserved 5 base pair sequence (ACGTG) was identified in central nervous system midline transcriptional enhancers of three genes. Germ-line transformation experiments indicate that this motif forms the core of an element required for central nervous system midline transcription. The central nervous system midline element is related to the mammalian xenobiotic response element, which regulates transcription of genes that metabolize aromatic hydrocarbons. These data suggest a model whereby related basic-helix-loop-helix-PAS proteins interact with asymmetric E-box-like target sequences to control these disparate processes.

Development ◽  
1994 ◽  
Vol 120 (1) ◽  
pp. 123-133 ◽  
Author(s):  
T.V. Menne ◽  
C. Klambt

The commissures of the Drosophila central nervous system (CNS) are formed in close relation to the ventral midline cells, a morphologically distinct set of cells located at the midline of the developing CNS. To analyze the function of these cells during commissure formation, we looked for mutations that result in the absence of commissures. One example of a gene that can give rise to such a phenotype is the neurogenic gene Notch. Here we show that mutant Notch embryos are devoid of commissural connections and have an abnormal midline. The midline cells of the embryonic Drosophila CNS are specified during the blastoderm stage about two hours before the first neuroblasts start to delaminate from the neurogenic region. To analyze Notch function for commissure development further, we took advantage of the Notchts1 allele. Temperature-shift experiments demonstrated that the lack of commissures in mutant Notch embryos results from defects in the analage of the CNS midline cells. Here maternal as well as zygotic Notch function are required for the correct activation of the gene single-minded, since mutant Notch embryos derived from germ-line clones lack most of the single-minded-positive midline cells.


Development ◽  
1997 ◽  
Vol 124 (17) ◽  
pp. 3263-3272 ◽  
Author(s):  
T. Roztocil ◽  
L. Matter-Sadzinski ◽  
C. Alliod ◽  
M. Ballivet ◽  
J.M. Matter

Genes encoding transcription factors of the helix-loop-helix family are essential for the development of the nervous system in Drosophila and vertebrates. Screens of an embryonic chick neural cDNA library have yielded NeuroM, a novel neural-specific helix-loop-helix transcription factor related to the Drosophila proneural gene atonal. The NeuroM protein most closely resembles the vertebrate NeuroD and Nex1/MATH2 factors, and is capable of transactivating an E-box promoter in vivo. In situ hybridization studies have been conducted, in conjunction with pulse-labeling of S-phase nuclei, to compare NeuroM to NeuroD expression in the developing nervous system. In spinal cord and optic tectum, NeuroM expression precedes that of NeuroD. It is transient and restricted to cells lining the ventricular zone that have ceased proliferating but have not yet begun to migrate into the outer layers. In retina, NeuroM is also transiently expressed in cells as they withdraw from the mitotic cycle, but persists in horizontal and bipolar neurons until full differentiation, assuming an expression pattern exactly complementary to NeuroD. In the peripheral nervous system, NeuroM expression closely follows cell proliferation, suggesting that it intervenes at a similar developmental juncture in all parts of the nervous system. We propose that availability of the NeuroM helix-loop-helix factor defines a new stage in neurogenesis, at the transition between undifferentiated, premigratory and differentiating, migratory neural precursors.


1994 ◽  
Vol 13 (8) ◽  
pp. 1799-1805 ◽  
Author(s):  
M. Ishibashi ◽  
K. Moriyoshi ◽  
Y. Sasai ◽  
K. Shiota ◽  
S. Nakanishi ◽  
...  

2004 ◽  
Vol 279 (16) ◽  
pp. 16356-16367 ◽  
Author(s):  
Tomoya Nakatani ◽  
Eri Mizuhara ◽  
Yasuko Minaki ◽  
Yoshimasa Sakamoto ◽  
Yuichi Ono

Development ◽  
2002 ◽  
Vol 129 (12) ◽  
pp. 2947-2956 ◽  
Author(s):  
Marios Georgiou ◽  
Guy Tear

In the absence of Commissureless (Comm) function, axons are unable to extend across the central nervous system midline. Comm downregulates levels of Roundabout (Robo), a receptor for the midline repellent Slit, in order to allow axons to cross the midline. comm transcript is expressed at high levels in the midline glia and Comm protein accumulates on axons at the midline. This has led to the hypothesis that Comm moves from the midline glia to the axons, where it can reduce Robo levels. We have found that expression of Comm in the midline cells is unable to rescue the comm phenotype and that tagged versions of Comm are not transferred to axons. A re-examination of Comm protein expression and the use of targeted RNA interference reveal that correct midline crossing requires that Comm is expressed in the commissural axons and midline glia. We suggest that accumulation of Comm protein at the midline spatially limits Comm activity and prevents it from being active on the contralateral side of the central nervous system.


Stem Cells ◽  
2009 ◽  
Vol 27 (4) ◽  
pp. 847-856 ◽  
Author(s):  
Cédric G. Geoffroy ◽  
James A. Critchley ◽  
Diogo S. Castro ◽  
Sandra Ramelli ◽  
Christelle Barraclough ◽  
...  

genesis ◽  
2007 ◽  
Vol 45 (5) ◽  
pp. 266-274 ◽  
Author(s):  
So Hee Kim ◽  
Hyeon Ju Kim ◽  
Soo Youn Kim ◽  
Sang-Hak Jeon ◽  
Sang Hee Kim

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