Expression domains of a zebrafish homologue of the Drosophila pair-rule gene hairy correspond to primordia of alternating somites

Development ◽  
1996 ◽  
Vol 122 (7) ◽  
pp. 2071-2078 ◽  
Author(s):  
M. Muller ◽  
E. Weizsacker ◽  
J.A. Campos-Ortega

her1 is a zebrafish cDNA encoding a bHLH protein with all features characteristic of members of the Drosophila HAIRY-E(SPL) family. During late gastrulation stages, her1 is expressed in the epibolic margin and in two distinct transverse bands of hypoblastic cells behind the epibolic front. After completion of epiboly, this pattern persists essentially unchanged through postgastrulation stages; the marginal domain is incorporated in the tail bud and, depending on the time point, either two or three paired bands of expressing cells are present within the paraxial presomitic mesoderm separated by regions devoid of transcripts. Labelling of cells within the her1 expression domains with fluorescein-dextran shows that the cells in the epibolic margin and the tail bud are not allocated to particular somites. However, allocation of cells to somites occurs between the marginal expression domain and the first expression band, anterior to it. Moreover, the her1 bands, and the intervening non-expressing zones, each represents the primordium of a somite. This expression pattern is highly reminiscent of that of Drosophila pair-rule genes. A possible participation of her1 in functions related to somite formation is discussed.

Development ◽  
1999 ◽  
Vol 126 (13) ◽  
pp. 3005-3014 ◽  
Author(s):  
C. Takke ◽  
J.A. Campos-Ortega

During vertebrate embryonic development, the paraxial mesoderm becomes subdivided into metameric units known as somites. In the zebrafish embryo, genes encoding homologues of the proteins of the Drosophila Notch signalling pathway are expressed in the presomitic mesoderm and expression is maintained in a segmental pattern during somitogenesis. This expression pattern suggests a role for these genes during somite development. We misexpressed various zebrafish genes of this group by injecting mRNA into early embryos. RNA encoding a constitutively active form of notch1a (notch1a-intra) and a truncated variant of deltaD [deltaD(Pst)], as well as transcripts of deltaC and deltaD, the hairy-E(spl) homologues her1 and her4, and groucho2 were tested for their effects on somite formation, myogenesis and on the pattern of transcription of putative downstream genes. In embryos injected with any of these RNAs, with the exception of groucho2 RNA, the paraxial mesoderm differentiated normally into somitic tissue, but failed to segment correctly. Activation of notch results in ectopic activation of her1 and her4. This misregulation of the expression of her genes might be causally related to the observed mesodermal defects, as her1 and her4 mRNA injections led to effects similar to those seen with notch1a-intra. deltaC and deltaD seem to function after subdivision of the presomitic mesoderm, since the her gene transcription pattern in the presomitic mesoderm remains essentially normal after misexpression of delta genes. Whereas notch signalling alone apparently does not affect myogenesis, zebrafish groucho2 is involved in differentiation of mesodermal derivatives.


2016 ◽  
Author(s):  
Rotem Lavy ◽  
W. Ted Allison ◽  
Fred B. Berry

AbstractSomitogenesis is a fundamental segmentation process that forms the vertebrate body plan. A network of transcription factors is essential in establishing the spatial temporal order of this process. One such transcription factor is mesp-ba which has an important role in determining somite boundary formation. Its expression in somitogenesis is tightly regulated by the transcriptional activator Tbx6 and the repressor Ripply1 via a feedback regulatory network. Loss of foxc1a function in zebrafish leads to lack of anterior somite formation and reduced mesp-ba expression. Here we examine how foxc1a interacts with the tbx6-ripply1 network to regulate mesp-ba expression. In foxc1a morphants, anterior somites did not form at 12.5 hours post fertilization (hpf). At 22 hpf posterior somites formed, whereas anterior somites remained absent. In ripply1 morphants, no somites were observed at any time point. The expression of mesp-ba was reduced in the foxc1a morphants and expanded anteriorly in ripply1 morphants. The tbx6 expression domain was smaller and shifted anteriorly in the foxc1a morphants. Double knockdown of foxc1a and ripply1 resulted in absence of anterior somite formation while posterior somites did form, suggesting a partial rescue of the ripply1 phenotype. However, unlike the single foxc1a morphants, expression of mesp-ba was restored in the anterior PSM. Expression of tbx6 was expanded anteriorly in the double morphants. In conclusion, both foxc1a and ripply1 morphants displayed defects in somitogenesis, but their individual loss of function had opposing effects on mesp-ba expression. Loss of ripply1 appears to have rescued the mesp-ba expression in the foxc1a morphant, suggesting that intersection of these parallel regulatory mechanisms is required for normal mesp-ba expression and somite formation.


Development ◽  
1981 ◽  
Vol 65 (Supplement) ◽  
pp. 103-128
Author(s):  
P. P. L. Tam

Somitogenesis in the mouse embryo commences with the generation of presumptive somitic mesoderm at the primitive streak and in the tail-bud mesenchyme. The presumptive somitic mesoderm is then organized into somite primordia in the presomitic mesoderm. These primordia undergo morphogenesis leading to the segmentation of somites at the cranial end of the presomitic mesoderm. Somite sizes at the time of segmentation vary according to the position of the somite in the body axis: the size of lumbar and sacral somites is nearly twice that of upper trunk somites and of tail somites. The size of the presomitic mesoderm, which is governed by the balance between the addition of cells at the caudal end and the removal of somites at the cranial end, changes during embryonic development. Somitogenesis is disturbed during the compensatory growth of mouse embryos which have suffered a drastic size reduction at the primitive-streak and early-organogenesis stages. The formation of somites is retarded and the upper trunk somites are formed at a smaller size. The embryo also follows an entirely different growth profile, but a normal body size is restored by the early foetal stage. The somite number is regulated to normal and this is brought about by an altered rate of somite formation and the adjustment of somite size in proportion to the whole body size. It is proposed that axis formation and somitogenesis are related morphogenetic processes and that embryonic growth controls the kinetics of somitogenesis, namely by regulating the number of cells allocated to each somite and the rate of somite formation.


Development ◽  
2001 ◽  
Vol 128 (24) ◽  
pp. 5139-5147
Author(s):  
Catarina Freitas ◽  
Sofia Rodrigues ◽  
Jean-Baptiste Charrier ◽  
Marie-Aimée Teillet ◽  
Isabel Palmeirim

In the vertebrate embryo, segmentation is built on repetitive structures, named somites, which are formed progressively from the most rostral part of presomitic mesoderm, every 90 minutes in the avian embryo. The discovery of the cyclic expression of several genes, occurring every 90 minutes in each presomitic cell, has shown that there is a molecular clock linked to somitogenesis. We demonstrate that a dynamic expression pattern of the cycling genes is already evident at the level of the prospective presomitic territory. The analysis of this expression pattern, correlated with a quail/chick fate-map, identifies a ‘wave’ of expression travelling along the future medial/lateral presomitic axis. Further analysis also reveals the existence of a medial/lateral asynchrony of expression at the level of presomitic mesoderm. This work suggests that the molecular clock is providing cellular positional information not only along the anterior/posterior but also along the medial/lateral presomitic axis. Finally, by using an in vitro culture system, we show that the information for morphological somite formation and molecular segmentation is segregated within the medial/lateral presomitic axis. Medial presomitic cells are able to form somites and express segmentation markers in the absence of lateral presomitic cells. By contrast, and surprisingly, lateral presomitic cells that are deprived of their medial counterparts are not able to organise themselves into somites and lose the expression of genes known to be important for vertebrate segmentation, such as Delta-1, Notch-1, paraxis, hairy1, hairy2 and lunatic fringe.


2018 ◽  
Vol 2018 ◽  
pp. 1-13
Author(s):  
Wei Huang ◽  
Yu Zhang ◽  
Kang Cao ◽  
Lingfei Luo ◽  
Sizhou Huang

During somitogenesis, Fgf8 maintains the predifferentiation stage of presomitic mesoderm (PSM) cells and its retraction gives a cue for somite formation. Delta/Notch initiates the expression of oscillation genes in the tail bud and subsequently contributes to somite formation in a periodic way. Whether there exists a critical factor coordinating Fgf8 and Notch signaling pathways is largely unknown. Here, we demonstrate that the loss of function of geminin gave rise to narrower somites as a result of derepressed Fgf8 gradient in the PSM and tail bud. Furthermore, in geminin morphants, the somite boundary could not form properly but the oscillation of cyclic genes was normal, displaying the blurry somitic boundary and disturbed somite polarity along the AP axis. In mechanism, these manifestations were mediated by the disrupted association of the geminin/Brg1 complex with intron 3 of mib1. The latter interaction was found to positively regulate mib1 transcription, Notch activity, and sequential somite segmentation during somitogenesis. In addition, geminin was also shown to regulate the expression of deltaD in mib1-independent way. Collectively, our data for the first time demonstrate that geminin regulates Fgf8 and Notch signaling to regulate somite segmentation during somitogenesis.


2000 ◽  
Vol 14 (13) ◽  
pp. 1678-1690 ◽  
Author(s):  
Scott A. Holley ◽  
Robert Geisler ◽  
Christiane Nüsslein-Volhard

Somitogenesis has been linked both to a molecular clock that controls the oscillation of gene expression in the presomitic mesoderm (PSM) and to Notch pathway signaling. The oscillator, or clock, is thought to create a prepattern of stripes of gene expression that regulates the activity of the Notch pathway that subsequently directs somite border formation. Here, we report that the zebrafish gene after eight (aei) that is required for both somitogenesis and neurogenesis encodes the Notch ligand DeltaD. Additional analysis revealed that stripes of her1 expression oscillate within the PSM and that aei/DeltaDsignaling is required for this oscillation.aei/DeltaD expression does not oscillate, indicating that the activity of the Notch pathway upstream ofher1 may function within the oscillator itself. Moreover, we found that her1 stripes are expressed in the anlage of consecutive somites, indicating that its expression pattern is not pair-rule. Analysis of her1 expression inaei/DeltaD, fused somites (fss), and aei;fss embryos uncovered a wave-front activity that is capable of continually inducing her1 expression de novo in the anterior PSM in the absence of the oscillation of her1. The wave-front activity, in reference to the clock and wave-front model, is defined as such because it interacts with the oscillator-derived pattern in the anterior PSM and is required for somite morphogenesis. This wave-front activity is blocked in embryos mutant for fssbut not aei/DeltaD. Thus, our analysis indicates that the smooth sequence of formation, refinement, and fading ofher1 stripes in the PSM is governed by two separate activities.


Development ◽  
1997 ◽  
Vol 124 (7) ◽  
pp. 1343-1354 ◽  
Author(s):  
D. Kosman ◽  
S. Small

The asymmetric distribution of the gap gene knirps (kni) in discrete expression domains is critical for striped patterns of pair-rule gene expression in the Drosophila embryo. To test whether these domains function as sources of morphogenetic activity, the stripe 2 enhancer of the pair-rule gene even-skipped (eve) was used to express kni in an ectopic position. Manipulating the stripe 2-kni expression constructs and examining transgenic lines with different insertion sites led to the establishment of a series of independent lines that displayed consistently different levels and developmental profiles of expression. Individual lines showed specific disruptions in pair-rule patterning that were correlated with the level and timing of ectopic expression. These results suggest that the ectopic domain acts as a source for morphogenetic activity that specifies regions in the embryo where pair-rule genes can be activated or repressed. Evidence is presented that the level and timing of expression, as well as protein diffusion, are important for determining the specific responses of target genes.


Development ◽  
1989 ◽  
Vol 106 (1) ◽  
pp. 173-183 ◽  
Author(s):  
A. Ruiz ◽  
i. Altaba ◽  
D.A. Melton

A Xenopus laevis homeobox gene, Xhox3, has been isolated using the homeobox of the Drosophila pair-rule gene even skipped as a hybridization probe. Xhox3 is first transcribed at the midblastula transition; RNA levels peak at the early neurula stage and decrease thereafter. During the early period of Xhox3 expression, the gastrula and neurula stages, transcripts are found in a graded fashion along the anteroposterior (A-P) axis in the mesoderm and are most concentrated at the posterior pole. In the late period of expression, the tailbud and tadpole stage, transcripts are concentrated at the two ends of the embryo: in the anterior nervous system and posterior tail bud. Analysis of Xhox3 expression in experimentally perturbed embryos shows that different A-P fates in the mesoderm are correlated with different levels of Xhox3 expression. Based on these results and those with other frog homeobox genes, we propose a role for homeobox genes in the patterning of the A-P embryonic axis.


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