scholarly journals Spatial regulation of the gap gene giant during Drosophila development

Development ◽  
1991 ◽  
Vol 111 (2) ◽  
pp. 601-609 ◽  
Author(s):  
R. Kraut ◽  
M. Levine
Keyword(s):  
Gene Dosage ◽  
Early Embryo ◽  
Early Embryogenesis ◽  
Maternal Factors ◽  
Spatial Regulation ◽  
Gap Gene ◽  
Gap Genes ◽  
Regulated Expression ◽  
Bona Fide ◽  
Protein Gradients

We describe the regulated expression of the segmentation gene giant (gt) during early embryogenesis. The gt protein is expressed in two broad gradients in precellular embryos, one in anterior regions and the other in posterior regions. Double immunolocalization studies show that the gt patterns overlap with protein gradients specified by the gap genes hunchback (hb) and knirps (kni). Analysis of all known gap mutants, as well as mutations that disrupt each of the maternal organizing centers, indicate that maternal factors are responsible for initiating gt expression, while gap genes participate in the subsequent refinement of the pattern. The maternal morphogen bicoid (bcd) initiates the anterior gt pattern, while nanos (nos) plays a role in the posterior pattern. Gene dosage studies indicate that different thresholds of the bcd gradient might trigger hb and gt expression, resulting in overlapping but noncoincident patterns of expression. We also present evidence that different concentrations of hb protein are instructive in defining the limits of kni and gt expression within the presumptive abdomen. These results suggest that gt is a bona fide gap gene, which acts with hb, Kruppel and kni to initiate striped patterns of gene expression in the early embryo.

Mutually repressive interactions between the gap genes giant and Kruppel define middle body regions of the Drosophila embryo

Development ◽  
1991 ◽  
Vol 111 (2) ◽  
pp. 611-621 ◽  
Author(s):  
R. Kraut ◽  
M. Levine
Keyword(s):  
Gene Expression ◽  
Weak Interactions ◽  
Ectopic Expression ◽  
Early Embryo ◽  
Drosophila Embryo ◽  
Regulatory Interactions ◽  
Gap Gene ◽  
Gap Genes ◽  
Body Regions ◽  
Bona Fide

The gap genes play a key role in establishing pair-rule and homeotic stripes of gene expression in the Drosophila embryo. There is mounting evidence that overlapping gradients of gap gene expression are crucial for this process. Here we present evidence that the segmentation gene giant is a bona fide gap gene that is likely to act in concert with hunchback, Kruppel and knirps to initiate stripes of gene expression. We show that Kruppel and giant are expressed in complementary, non-overlapping sets of cells in the early embryo. These complementary patterns depend on mutually repressive interactions between the two genes. Ectopic expression of giant in early embryos results in the selective repression of Kruppel, and advanced-stage embryos show cuticular defects similar to those observed in Kruppel- mutants. This result and others suggest that the strongest regulatory interactions occur among those gap genes expressed in nonadjacent domains. We propose that the precisely balanced overlapping gradients of gap gene expression depend on these strong regulatory interactions, coupled with weak interactions between neighboring genes.

scholarly journals tarsal-less is expressed as a gap gene but has no gap gene phenotype in the moth midge Clogmia albipunctata

2018 ◽  
Vol 5 (8) ◽  
pp. 180458 ◽  
Author(s):  
Eva Jiménez-Guri ◽  
Karl R. Wotton ◽  
Johannes Jaeger
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Rna Interference ◽  
Gap Gene ◽  
Gap Genes ◽  
Subtle Effect ◽  
Bona Fide ◽  
Vinegar Fly ◽  
Clogmia Albipunctata ◽  
Overlapping Domains

Gap genes are involved in segment determination during early development of the vinegar fly Drosophila melanogaster and other dipteran insects (flies, midges and mosquitoes). They are expressed in overlapping domains along the antero-posterior (A–P) axis of the blastoderm embryo. While gap domains cover the entire length of the A–P axis in Drosophila, there is a region in the blastoderm of the moth midge Clogmia albipunctata , which lacks canonical gap gene expression. Is a non-canonical gap gene functioning in this area? Here, we characterize tarsal-less ( tal ) in C. albipunctata . The homologue of tal in the flour beetle Tribolium castaneum (called milles-pattes, mlpt ) is a bona fide gap gene. We find that Ca-tal is expressed in the region previously reported as lacking gap gene expression. Using RNA interference, we study the interaction of Ca-tal with gap genes. We show that Ca-tal is regulated by gap genes, but only has a very subtle effect on tailless (Ca-tll), while not affecting other gap genes at all. Moreover, cuticle phenotypes of Ca-tal depleted embryos do not show any gap phenotype. We conclude that Ca-tal is expressed and regulated like a gap gene, but does not function as a gap gene in C. albipunctata .

scholarly journals tarsal-less is expressed as a gap gene but has no gap gene phenotype in the moth midge Clogmia albipunctata

2018 ◽  
Author(s):  
Eva Jiménez-Guri ◽  
Karl R. Wotton ◽  
Johannes Jaeger
Keyword(s):  
Gene Expression ◽  
Drosophila Melanogaster ◽  
Rna Interference ◽  
Gap Gene ◽  
Gap Genes ◽  
Subtle Effect ◽  
Bona Fide ◽  
Vinegar Fly ◽  
Clogmia Albipunctata ◽  
Overlapping Domains

AbstractGap genes are involved in segment determination during early development of the vinegar fly Drosophila melanogaster and other dipteran insects (flies, midges, and mosquitoes). They are expressed in overlapping domains along the antero-posterior (A–P) axis of the blastoderm embryo. While gap domains cover the entire length of the A–P axis in Drosophila, there is a region in the blastoderm of the moth midge Clogmia albipunctata, which lacks canonical gap gene expression. Is a non-canonical gap gene functioning in this area? Here, we characterize tarsal-less (tal) in C. albipunctata. The homolog of tal in the flour beetle Tribolium castaneum (called milles-pattes, mlpt) is a bona fide gap gene. We find that Ca-tal is expressed in the region previously reported as lacking gap gene expression. Using RNA interference, we study the interaction of Ca-tal with gap genes. We show that Ca-tal is regulated by gap genes, but only has a very subtle effect on tailless (Catll), while not affecting other gap genes at all. Moreover, cuticle phenotypes of Ca-tal depleted embryos do not show any gap phenotype. We conclude that Ca-tal is expressed and regulated like a gap gene, but does not function as a gap gene in C. albipunctata.

Different levels of Ras activity can specify distinct transcriptional and morphological consequences in early Drosophila embryos

Development ◽  
1997 ◽  
Vol 124 (23) ◽  
pp. 4879-4886 ◽  
Author(s):  
S. Greenwood ◽  
G. Struhl
Keyword(s):  
Signal Transduction Pathway ◽  
Early Embryo ◽  
Posterior Pole ◽  
The Body ◽  
Gap Gene ◽  
Gap Genes ◽  
Low Levels ◽  
Ras Signal Transduction ◽  
Different Levels ◽  
Drosophila Embryos

The terminal portions of the Drosophila body pattern are specified by the localized activity of the receptor tyrosine kinase Torso (Tor) at each pole of the early embryo. Tor activity elicits the transcription of two ‘gap’ genes, tailless (tll) and huckebein (hkb), in overlapping but distinct domains by stimulating the Ras signal transduction pathway. Here, we show that quantitative variations in the level of Ras activity can specify qualitatively distinct transcriptional and morphological responses. Low levels of Ras activity at the posterior pole direct tll but not hkb transcription; higher levels drive transcription of both genes. Correspondingly, low levels of Ras activity specify a limited subset of posterior terminal structures, whereas higher levels specify a larger subset. However, we also show that the response to Ras activity is not uniform along the body. Instead, levels of Ras activity which suffice to drive tll and hkb transcription at the posterior pole fail to drive their expression in more central portions of the body, apparently due to repression by other gap gene products. We conclude that tll and hkb transcription, as well as the terminal structures, are specified by two inputs: a gradient of Ras activity which emanates from the pole, and the opposing influence of more centrally deployed gap genes which repress the response to Ras.

Two distinct mechanisms for differential positioning of gene expression borders involving the Drosophila gap protein giant

Development ◽  
1998 ◽  
Vol 125 (19) ◽  
pp. 3765-3774 ◽  
Author(s):  
X. Wu ◽  
R. Vakani ◽  
S. Small
Keyword(s):  
Target Genes ◽  
Early Embryo ◽  
Drosophila Embryo ◽  
Anterior Border ◽  
Gap Gene ◽  
Gap Genes ◽  
Pair Rule Gene ◽  
Differential Positioning ◽  
Pair Rule

We have combined genetic experiments and a targeted misexpression approach to examine the role of the gap gene giant (gt) in patterning anterior regions of the Drosophila embryo. Our results suggest that gt functions in the repression of three target genes, the gap genes Kruppel (Kr) and hunchback (hb), and the pair-rule gene even-skipped (eve). The anterior border of Kr, which lies 4–5 nucleus diameters posterior to nuclei that express gt mRNA, is set by a threshold repression mechanism involving very low levels of gt protein. In contrast, gt activity is required, but not sufficient for formation of the anterior border of eve stripe 2, which lies adjacent to nuclei that express gt mRNA. We propose that gt's role in forming this border is to potentiate repressive interaction(s) mediated by other factor(s) that are also localized to anterior regions of the early embryo. Finally, gt is required for repression of zygotic hb expression in more anterior regions of the embryo. The differential responses of these target genes to gt repression are critical for the correct positioning and maintenance of segmentation stripes, and normal anterior development.

An activity gradient of decapentaplegic is necessary for the specification of dorsal pattern elements in the Drosophila embryo

Development ◽  
1993 ◽  
Vol 117 (2) ◽  
pp. 807-822 ◽  
Author(s):  
K.A. Wharton ◽  
R.P. Ray ◽  
W.M. Gelbart
Keyword(s):  
Cell Fate ◽  
Gene Dosage ◽  
Early Embryo ◽  
Drosophila Embryo ◽  
Cell Fates ◽  
Gene Encoding ◽  
In The Wild ◽  
Intercellular Signalling ◽  
Overlapping Domains ◽  
Dorsal Pattern

decapentaplegic (dpp) is a zygotically expressed gene encoding a TGF-beta-related ligand that is necessary for dorsal-ventral patterning in the Drosophila embryo. We show here that dpp is an integral part of a gradient that specifies many different cell fates via intercellular signalling. There is a graded requirement for dpp activity in the early embryo: high levels of dpp activity specify the amnioserosa, while progressively lower levels specify dorsal and lateral ectoderm. This potential for dpp to specify cell fate is highly dosage sensitive. In the wild-type embryo, increasing the gene dosage of dpp can shift cell fates along the dorsal-ventral axis. Furthermore, in mutant embryos, in which only a subset of the dorsal-ventral pattern elements are represented, increasing the gene dosage of dpp can specifically transform those pattern elements into more dorsal ones. We present evidence that the zygotic dpp gradient and the maternal dorsal gradient specify distinct, non-overlapping domains of the dorsal-ventral pattern.

scholarly journals A Role for RIC-8 (Synembryn) and GOA-1 (Goα) in Regulating a Subset of Centrosome Movements During Early Embryogenesis in Caenorhabditis elegans

Genetics ◽  
2000 ◽  
Vol 156 (4) ◽  
pp. 1649-1660
Author(s):  
Kenneth G Miller ◽  
James B Rand
Keyword(s):  
Caenorhabditis Elegans ◽  
Mitotic Spindle ◽  
Gene Dosage ◽  
Signal Transduction Pathway ◽  
Nuclear Migration ◽  
Early Embryogenesis ◽  
Embryonic Lethality ◽  
Neurotransmitter Secretion ◽  
Embryonic Polarity ◽  
Neuronal Signal

Abstract RIC-8 (synembryn) and GOA-1 (Goα) are key components of a signaling network that regulates neurotransmitter secretion in Caenorhabditis elegans. Here we show that ric-8 and goa-1 reduction of function mutants exhibit partial embryonic lethality. Through Nomarski analysis we show that goa-1 and ric-8 mutant embryos exhibit defects in multiple events that involve centrosomes, including one-cell posterior centrosome rocking, P1 centrosome flattening, mitotic spindle alignment, and nuclear migration. In ric-8 reduction of function backgrounds, the embryonic lethality, spindle misalignments and delayed nuclear migration are strongly enhanced by a 50% reduction in maternal goa-1 gene dosage. Several other microfilament- and microtubule-mediated events, as well as overall embryonic polarity, appear unperturbed in the mutants. In addition, our results suggest that RIC-8 and GOA-1 do not have roles in centrosome replication, in the diametric movements of daughter centrosomes along the nuclear membrane, or in the extension of microtubules from centrosomes. Through immunostaining we show that GOA-1 (Goα) localizes to cell cortices as well as near centrosomes. Our results demonstrate that two components of a neuronal signal transduction pathway also play a role in centrosome movements during early embryogenesis.

Posterior stripe expression of hunchback is driven from two promoters by a common enhancer element

Development ◽  
1995 ◽  
Vol 121 (9) ◽  
pp. 3067-3077 ◽  
Author(s):  
J.S. Margolis ◽  
M.L. Borowsky ◽  
E. Steingrimsson ◽  
C.W. Shim ◽  
J.A. Lengyel ◽  
...  
Keyword(s):  
Transcription Initiation ◽  
Initiation Site ◽  
Drosophila Embryo ◽  
Upstream Region ◽  
Enhancer Element ◽  
Gap Gene ◽  
Gap Genes ◽  
Two Phases ◽  
Necessary And Sufficient

The gap gene hunchback (hb) is required for the formation and segmentation of two regions of the Drosophila embryo, a broad anterior domain and a narrow posterior domain. Accumulation of hb transcript in the posterior of the embryo occurs in two phases, an initial cap covering the terminal 15% of the embryo followed by a stripe at the anterior edge of this region. By in situ hybridization with transcript-specific probes, we show that the cap is composed only of mRNA from the distal transcription initiation site (P1), while the later posterior stripe is composed of mRNA from both the distal and proximal (P2) transcription initiation sites. Using a series of genomic rescue constructs and promoter-lacZ fusion genes, we define a 1.4 kb fragment of the hb upstream region that is both necessary and sufficient for posterior expression. Sequences within this fragment mediate regulation by the terminal gap genes tailless (tll) and a huckebein, which direct the formation of the posterior hb stripe. We show that the tll protein binds in vitro to specific sites within the 1.4 kb posterior enhancer region, providing the first direct evidence for activation of gene expression by tll. We propose a model in which the anterior border of the posterior hb stripe is determined by tll concentration in a manner analogous to the activation of anterior hb expression by bicoid.

scholarly journals AtNSE1 and AtNSE3 are required for embryo pattern formation and maintenance of cell viability during Arabidopsis embryogenesis

2019 ◽  
Vol 70 (21) ◽  
pp. 6229-6244
Author(s):  
Gang Li ◽  
Wenxuan Zou ◽  
Liufang Jian ◽  
Jie Qian ◽  
Jie Zhao
Keyword(s):  
Cell Death ◽  
Cell Viability ◽  
Cell Fate ◽  
Embryo Development ◽  
Higher Plants ◽  
Early Embryo ◽  
Embryo Cell ◽  
Early Embryogenesis ◽  
Embryo Abortion ◽  
Cell Fate Decisions

Abstract Embryogenesis is an essential process during seed development in higher plants. It has previously been shown that mutation of the Arabidopsis non-SMC element genes AtNSE1 or AtNSE3 leads to early embryo abortion, and their proteins can interact with each other directly. However, the crucial regions of these proteins in this interaction and how the proteins are cytologically involved in Arabidopsis embryo development are unknown. In this study, we found that the C-terminal including the Ring-like motif of AtNSE1 can interact with the N-terminal of AtNSE3, and only the Ring-like motif is essential for binding with three α motifs of AtNSE2 (homologous to AtMMS21). Using genetic assays and by analysing molecular markers of cell fate decisions (STM, WOX5, and WOX8) in mutant nse1 and nse3 embryos, we found that AtNSE1 and AtNSE3 work non-redundantly in early embryo development, and that differentiation of the apical meristem and the hypophysis fails in the mutants, which have disrupted auxin transportation and responses. However, the upper cells of the suspensor in the mutants seem to have proper embryo cell identity. Cytological examination showed that cell death occurred from the early embryo stage, and that vacuolar programmed cell death and necrosis in the nse1 and nse3 mutant embryos led to ovule abortion. Thus, AtNSE1 and AtNSE3 are essential for maintaining cell viability and growth during early embryogenesis. Our results improve our understanding of the functions of SMC5/6 complex in early embryogenesis in Arabidopsis.

scholarly journals Female Mice Haploinsufficient for an Inactivated Androgen Receptor (AR) Exhibit Age-Dependent Defects That Resemble the AR Null Phenotype of Dysfunctional Late Follicle Development, Ovulation, and Fertility

Endocrinology ◽  
2007 ◽  
Vol 148 (8) ◽  
pp. 3674-3684 ◽  
Author(s):  
K. A. Walters ◽  
C. M. Allan ◽  
M. Jimenez ◽  
P. R. Lim ◽  
R. A. Davey ◽  
...  
Keyword(s):  
Androgen Receptor ◽  
Ovarian Function ◽  
Gene Dosage ◽  
Early Embryo ◽  
Ovulation Rate ◽  
Corpora Lutea ◽  
Cell Stage ◽  
Gene Dosage Effect ◽  
Female Mice ◽  
Age Dependent

The role of classical genomic androgen receptor (AR) mediated actions in female reproductive physiology remains unclear. Female mice homozygous for an in-frame deletion of exon 3 of the Ar (AR−/−) were subfertile, exhibiting delayed production of their first litter (AR+/+ = 22 d vs. AR−/− = 61 d, P < 0.05) and producing 60% fewer pups/litter (AR+/+: 8.1 ± 0.4 vs. AR−/−: 3.2 ± 0.9, P < 0.01). Heterozygous females (AR+/−) exhibited an age-dependent 55% reduction (P < 0.01) in pups per litter, evident from 6 months of age (P < 0.05), compared with AR+/+, indicating a significant gene dosage effect on female fertility. Ovulation was defective with a significant reduction in corpora lutea numbers (48–79%, P < 0.01) in 10- to 12- and 26-wk-old AR+/− and AR−/− females and a 57% reduction in oocytes recovered from naturally mated AR−/− females (AR+/+: 9.8 ± 1.0 vs. AR−/−: 4.2 ± 1.2, P < 0.01); however, early embryo development to the two-cell stage was unaltered. The delay in first litter, reduction in natural ovulation rate, and aromatase expression in AR+/− and AR−/− ovaries, coupled with the restored ovulation rate by gonadotropin hyperstimulation in AR−/− females, suggest aberrant gonadotropin regulation. A 2.7-fold increase (AR+/+: 35.4 ± 13.4 vs. AR−/−: 93.9 ± 6.1, P < 0.01) in morphologically unhealthy antral follicles demonstrated deficiencies in late follicular development, although growing follicle populations and growth rates were unaltered. This novel model reveals that classical genomic AR action is critical for normal ovarian function, although not for follicle depletion and that haploinsufficiency for an inactivated AR may contribute to a premature reduction in female fecundity.

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