scholarly journals scute (sis-b) function in Drosophila sex determination.

1995 ◽  
Vol 15 (8) ◽  
pp. 4430-4440 ◽  
Author(s):  
G Deshpande ◽  
J Stukey ◽  
P Schedl
Keyword(s):  
Sex Determination ◽  
X Chromosome ◽  
Immunoblot Analysis ◽  
Lethal Gene ◽  
Helix Loop Helix ◽  
Nuclear Cycle ◽  
Early Embryos ◽  
Initial Activation ◽  
Activity State

The primary sex determination signal, the X chromosome-to-autosome (X/A) ratio, controls the choice of sexual identity in the Drosophila melanogaster embryo by regulating the activity of the early promoter of the Sex-lethal gene, Sxl-Pe. This promoter is activated in females (2X/2A), while it remains off in males (1X/2A). Promoter activation in females is dependent upon X-linked numerator genes. One of these genes, sisterless-b (sis-b), corresponds to the scute (sc) locus of the achaete-scute complex, and it encodes a helix-loop-helix transcription factor. In the studies reported here we have used monoclonal antibodies to study the expression and functioning of the sc(sis-b) protein. Sc is first detected at nuclear cycle 6 to 7, well before Sxl-Pe is first active. At this stage, the protein is in the cytoplasm, not the nucleus. Only after the formation of the syncytial blastoderm, at nuclear cycle 10 to 11, does a substantial fraction of the protein enter the nucleus, and this nuclear import closely coincides with the initial activation of Sxl-Pe. Consistent with the idea that the dose of sc(sis-b) is critical for its function as an X-chromosome counting element, wild-type syncytial blastoderm embryos could be grouped into two classes based on the level of protein. Western blot (immunoblot) analysis demonstrates that this difference in protein level correlates directly with the activity state of the Sxl gene. Finally, we provide the first direct evidence that Sc forms heteromeric complexes in vivo in early embryos with the maternally derived helix-loop-helix protein Daughterless. This in vivo complex is likely to be critical for Sc function in Sxl-Pe activation.

scholarly journals Differential effects of Sex-lethal mutations on dosage compensation early in Drosophila development.

Genetics ◽  
1994 ◽  
Vol 136 (3) ◽  
pp. 1051-1061
Author(s):  
M Bernstein ◽  
T W Cline
Keyword(s):  
Sex Determination ◽  
X Chromosome ◽  
Dosage Compensation ◽  
Rna Splicing ◽  
Lethal Gene ◽  
Loss Of Function ◽  
Developmental Pathway ◽  
Pathway Choice ◽  
Sex Lethal ◽  
Blastoderm Stage

Abstract In response to the primary sex determination signal, X chromosome dose, the Sex-lethal gene controls all aspects of somatic sex determination and differentiation, including X chromosome dosage compensation. Two complementary classes of mutations have been identified that differentially affect Sxl somatic functions: (1) those impairing the "early" function used to set developmental pathway choice in response to the sex determination signal and (2) those impairing "late" functions involved in maintaining the pathway choice independent of the initiating signal and/or in directing differentiation. This "early vs. late" distinction correlates with a switch in promoter utilization from SxlPe to SxlPm at the blastoderm stage and a corresponding switch from transcriptional to RNA splicing control. Here we characterize five partial-loss-of-function Sxl alleles to explore a distinction between "early vs. late" functioning of Sxl in dosage compensation. Assaying for dosage compensation during the blastoderm stage, we find that the earliest phase of the dosage compensation process is controlled by products of the early Sxl promoter, SxlPe. Hence, in addition to triggering the sexual pathway decision of cells, products derived from SxlPe also control early dosage compensation, the first manifestation of sexually dimorphic differentiation. The effects of mutant Sxl alleles on early dosage compensation are consistent with their previous categorization as early vs. late defective with respect to their effects on pathway initiation. Results reported here suggest that the dosage compensation regulatory genes currently known to function downstream of Sxl, genes known as the "male-specific lethals," do not control all aspects of dosage compensation either at the blastoderm stage or later in development. In the course of this study, we also discovered that the canonical early defective allele, Sxlf9, which is impaired in its ability to establish the female developmental pathway commitment, is likely to be defective in the stability and/or functioning of products derived from SxlPe, rather than in the ability of SxlPe to respond to the chromosomal sex determination signal.

scholarly journals Identification of putative c-Myc-responsive genes: characterization of rcl, a novel growth-related gene.

1997 ◽  
Vol 17 (9) ◽  
pp. 4967-4978 ◽  
Author(s):  
B C Lewis ◽  
H Shim ◽  
Q Li ◽  
C S Wu ◽  
L A Lee ◽  
...  
Keyword(s):  
Leucine Zipper ◽  
Cellular Proliferation ◽  
Ectopic Expression ◽  
Immunoblot Analysis ◽  
Lymphoid Cells ◽  
Representational Difference Analysis ◽  
Anchorage Independent Growth ◽  
Cdna Sequences ◽  
Helix Loop Helix

The c-Myc protein is a helix-loop-helix leucine zipper oncogenic transcription factor that participates in the regulation of cell proliferation, differentiation, and apoptosis. The biochemical function of c-Myc has been well described, yet the identities of downstream effectors are just beginning to emerge. We describe the identification of a set of c-Myc-responsive genes in the Rat1a fibroblast through the application of cDNA representational difference analysis (RDA) to cDNAs isolated from nonadherent Rat1a and Rat1a-myc cells. In this system, c-Myc overexpression is sufficient to induce the transformed phenotype of anchorage-independent growth. We identified 20 differentially expressed cDNAs, several of which represent novel cDNA sequences. We further characterized one of the novel cDNAs identified in this screen, termed rcl. rcl expression is (i) directly stimulated by c-Myc; (ii) stimulated in the in vivo growth system of regenerating rat liver, as is c-myc; and (iii) elevated in human lymphoid cells that overexpress c-myc. By using an anti-Rcl antibody, immunoblot analysis, and immunofluorescence microscopy, the Rcl protein was found to be a 23-kDa nuclear protein. Ectopic expression of the protein encoded by the rcl cDNA induces anchorage-independent growth in Rat1a fibroblasts, albeit to a diminished extent compared to ectopic c-Myc expression. These data suggest a role for rcl during cellular proliferation and c-Myc-mediated transformation.

Relaxation of Orthodontic Elastomeric Chains and Modules In Vitro and In Vivo

1978 ◽  
Vol 57 (5-6) ◽  
pp. 685-690 ◽  
Author(s):  
J.L. Ash ◽  
R.J. Nikolai
Keyword(s):  
Water Bath ◽  
Dry Air ◽  
Initial Activation ◽  
Elastomeric Chains

Relaxation patterns for two orthodontic polyurethane-based elastics have been quantified in dry air and water bath environments and in vivo. Water bath simulation of in vivo behavior is apparently valid for up to a week following initial activation, but it becomes somewhat erroneous thereafter.

Differential use of SCL/TAL-1 DNA-binding domain in developmental hematopoiesis

Blood ◽  
2008 ◽  
Vol 112 (4) ◽  
pp. 1056-1067 ◽  
Author(s):  
Mira T. Kassouf ◽  
Hedia Chagraoui ◽  
Paresh Vyas ◽  
Catherine Porcher
Keyword(s):  
Dna Binding ◽  
Molecular Mechanisms ◽  
Binding Activity ◽  
Hematopoietic Stem ◽  
Helix Loop Helix ◽  
Experimental Systems ◽  
Dna Binding Activity ◽  
Independent Functions

Abstract Dissecting the molecular mechanisms used by developmental regulators is essential to understand tissue specification/differentiation. SCL/TAL-1 is a basic helix-loop-helix transcription factor absolutely critical for hematopoietic stem/progenitor cell specification and lineage maturation. Using in vitro and forced expression experimental systems, we previously suggested that SCL might have DNA-binding–independent functions. Here, to assess the requirements for SCL DNA-binding activity in vivo, we examined hematopoietic development in mice carrying a germline DNA-binding mutation. Remarkably, in contrast to complete absence of hematopoiesis and early lethality in scl-null embryos, specification of hematopoietic cells occurred in homozygous mutant embryos, indicating that direct DNA binding is dispensable for this process. Lethality was forestalled to later in development, although some mice survived to adulthood. Anemia was documented throughout development and in adulthood. Cellular and molecular studies showed requirements for SCL direct DNA binding in red cell maturation and indicated that scl expression is positively autoregulated in terminally differentiating erythroid cells. Thus, different mechanisms of SCL's action predominate depending on the developmental/cellular context: indirect DNA binding activities and/or sequestration of other nuclear regulators are sufficient in specification processes, whereas direct DNA binding functions with transcriptional autoregulation are critically required in terminal maturation processes.

Major sex-determining genes and the control of sexual dimorphism in Caenorhabditis elegans

Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 625-637 ◽  
Author(s):  
Jonathan Hodgkin ◽  
Andrew D. Chisholm ◽  
Michael M. Shen
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Germ Line ◽  
Cell Lineage ◽  
Regulatory Genes ◽  
Nematode Caenorhabditis Elegans ◽  
X Chromosomes ◽  
The Many ◽  
Lineage Analysis

Sex determination in Caenorhabditis elegans involves a cascade of major regulatory genes connecting the primary sex determining signal, X chromosome dosage, to key switch genes, which in turn direct development along either male or female pathways. Animals with one X chromosome (XO) are male, while animals with two X chromosomes (XX) are hermaphrodite: hermaphrodite development occurs because the action of the regulatory genes is modified in the germ line so that both sperm and oocytes are made inside a completely female soma. The regulatory genes are being examined by both genetic and molecular means. We discuss how these major genes, in particular the last switch gene in the cascade, tra-1, might regulate the many different sex-specific events that occur during the development of the hermaphrodite and of the male.Key words: nematode, Caenorhabditis elegans, sex determination, sexual differentiation, cell lineage analysis.

Distribution of sister chromatid exchanges on the mouse chromosomes in vivo with reference to the replication properties of the X chromosome

1984 ◽  
Vol 26 (2) ◽  
pp. 152-157
Author(s):  
S. M. Singh ◽  
D. L. Reimer
Keyword(s):  
Bone Marrow ◽  
X Chromosome ◽  
Sister Chromatid ◽  
Bone Marrow Cells ◽  
Relative Length ◽  
Chromosome Length ◽  
Sister Chromatid Exchanges ◽  
Chromatid Exchanges ◽  
Marrow Cells

Frequency of sister chromatid exchanges (SCE) were recorded separately for different chromosomes from bone marrow cells of female mice of the two genetic strains (C3H/S and C57BL/6J). SCEs were evaluated following different doses of 5-bromo-2′deoxyuridine (BrdU) as nine hourly i.p. injections. The SCE per cell increased with increasing BrdU doses which was slightly higher in C3H/S than in the C57BL/6J. SCEs per cell were variable at every treatment – strain combination, possibly reflecting the heterogeneous nature of the bone marrow cells. In general, there is a positive correlation between SCE per chromosome and the relative chromosome length. Total SCEs on one of the large chromosomes (most likely the X chromosome), however, are significantly higher than expected on the basis of relative length alone. Most of this increase is attributable to one of the homologues of this chromosome, which is not in synchrony with the rest of the chromosomes and may represent the late-replicating X. These results when viewed in the light of replication properties of the heterochromatinized X, suggest a direct involvement of DNA replication in SCE formation and may argue against the replication point as the sole site for the SCEs.Key words: sister chromatid exchange, BrdU, recombination, replication, X chromosome.

Specificity of Chromosome Damage Caused by the Rex Element of Drosophila melanogaster

Genetics ◽  
1996 ◽  
Vol 144 (1) ◽  
pp. 109-115 ◽  
Author(s):  
Leonard G Robbins
Keyword(s):  
Drosophila Melanogaster ◽  
Early Development ◽  
X Chromosome ◽  
Ribosomal Rna ◽  
Chromosome Damage ◽  
Genetic Element ◽  
Single Chromosome ◽  
Experimental Cross ◽  
Rdna Array ◽  
Early Embryos

Abstract Rex is a multicopy genetic element that maps within an X-linked ribosomal RNA gene (rDNA) array of D. melanogaster. Acting maternally, Rex causes recombination between rDNA arrays in a few percent of early embryos. With target chromosomes that contain two rDNA arrays, the exchanges either delete all of the material between the two arrays or invert the entire intervening chromosomal segment. About a third of the embryos produced by Rex homozygotes have cytologically visible chromosome damage, nearly always involving a single chromosome. Most of these embryos die during early development, displaying a characteristic apoptosis-like phenotype. An experiment that tests whether the cytologically visible damage is rDNA-specific is reported here. In this experiment, females heterozygous for Rex and an rDNA-deficient X chromosome were crossed to males of two genotypes. Some of the progeny from the experimental cross entirely lacked rDNA, while all of the progeny from the control cross had at least one rDNA array. A significantly lower frequency of early-lethal embryos in the experimental cross, proportionate to the fraction of rDNA-deficient embryos, demonstrates that Rex preferentially damages rDNA.

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