An extracellular activator of the Drosophila JAK/STAT pathway is a sex-determination signal element

Nature ◽  
2000 ◽  
Vol 405 (6789) ◽  
pp. 970-973 ◽  
Author(s):  
Louise Sefton ◽  
John R. Timmer ◽  
Yan Zhang ◽  
Florence Béranger ◽  
Thomas W. Cline
Keyword(s):  
Sex Determination ◽  
Signal Element ◽  
Stat Pathway

scholarly journals Structural basis for the function of SuhB as a transcription factor in ribosomal RNA synthesis

2019 ◽  
Vol 47 (12) ◽  
pp. 6488-6503 ◽  
Author(s):  
Yong-Heng Huang ◽  
Nelly Said ◽  
Bernhard Loll ◽  
Markus C Wahl
Keyword(s):  
Escherichia Coli ◽  
Ribosomal Rna ◽  
Rna Synthesis ◽  
Rna Folding ◽  
In Vitro Transcription ◽  
Structural Basis ◽  
Macromolecular Crystallography ◽  
Rna Transcription ◽  
Signal Element

AbstractRibosomal RNA synthesis in Escherichia coli involves a transcription complex, in which RNA polymerase is modified by a signal element on the transcript, Nus factors A, B, E and G, ribosomal protein S4 and inositol mono-phosphatase SuhB. This complex is resistant to ρ-dependent termination and facilitates ribosomal RNA folding, maturation and subunit assembly. The functional contributions of SuhB and their structural bases are presently unclear. We show that SuhB directly binds the RNA signal element and the C-terminal AR2 domain of NusA, and we delineate the atomic basis of the latter interaction by macromolecular crystallography. SuhB recruitment to a ribosomal RNA transcription complex depends on the RNA signal element but not on the NusA AR2 domain. SuhB in turn is required for stable integration of the NusB/E dimer into the complex. In vitro transcription assays revealed that SuhB is crucial for delaying or suppressing ρ-dependent termination, that SuhB also can reduce intrinsic termination, and that SuhB-AR2 contacts contribute to these effects. Together, our results reveal functions of SuhB during ribosomal RNA synthesis and delineate some of the underlying molecular interactions.

scholarly journals The Primary Sex Determination Signal of Caenorhabditis elegans

Genetics ◽  
1999 ◽  
Vol 152 (3) ◽  
pp. 999-1015 ◽  
Author(s):  
Ilil Carmi ◽  
Barbara J Meyer
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
Counting Process ◽  
Rna Binding ◽  
Nuclear Hormone Receptor ◽  
Chromosome Counting ◽  
Specific Expression ◽  
X Chromosomes ◽  
Signal Element ◽  
Complete Transformation

AbstractAn X chromosome counting process determines sex in Caenorhabditis elegans. The dose of X chromosomes is translated into sexual fate by a set of X-linked genes that together control the activity of the sex-determination and dosage-compensation switch gene, xol-1. The double dose of X elements in XX animals represses xol-1 expression, promoting the hermaphrodite fate, while the single dose of X elements in XO animals permits high xol-1 expression, promoting the male fate. Previous work has revealed at least four signal elements that repress xol-1 expression at two levels, transcriptional and post-transcriptional. The two molecularly characterized elements include an RNA binding protein and a nuclear hormone receptor homolog. Here we explore the roles of the two mechanisms of xol-1 repression and further investigate how the combined dose of X signal elements ensures correct, sex-specific expression of xol-1. By studying the effects of increases and decreases in X signal element dose on male and hermaphrodite fate, we demonstrate that signal elements repress xol-1 cumulatively, such that full repression of xol-1 in XX animals results from the combined effect of individual elements. Complete transformation from the hermaphrodite to the male fate requires a decrease in the dose of all four elements, from two copies to one. We show that both mechanisms of xol-1 repression are essential and act synergistically to keep xol-1 levels low in XX animals. However, increasing repression by one mechanism can compensate for loss of the other, demonstrating that each mechanism can exert significant xol-1 repression on its own. Finally, we present evidence suggesting that xol-1 activity can be set at intermediate levels in response to an intermediate X signal.

Identification of X chromosome regions in Caenorhabditis elegans that contain sex-determination signal elements.

Genetics ◽  
1994 ◽  
Vol 138 (4) ◽  
pp. 1105-1125
Author(s):  
C C Akerib ◽  
B J Meyer
Keyword(s):  
Caenorhabditis Elegans ◽  
Sex Determination ◽  
X Chromosome ◽  
Dosage Compensation ◽  
X Chromosomes ◽  
Sensitive Region ◽  
Signal Element ◽  
Number Of Genes ◽  
Mutant Phenotypes ◽  
Chromosome Regions

Abstract The primary sex-determination signal of Caenorhabditis elegans is the ratio of X chromosomes to sets of autosomes (X/A ratio). This signal coordinately controls both sex determination and X chromosome dosage compensation. To delineate regions of X that contain counted signal elements, we examined the effect on the X/A ratio of changing the dose of specific regions of X, using duplications in XO animals and deficiencies in XX animals. Based on the mutant phenotypes of genes that are controlled by the signal, we expected that increases (in males) or decreases (in hermaphrodites) in the dose of X chromosome elements could cause sex-specific lethality. We isolated duplications and deficiencies of specific X chromosome regions, using strategies that would permit their recovery regardless of whether they affect the signal. We identified a dose-sensitive region at the left end of X that contains X chromosome signal elements. XX hermaphrodites with only one dose of this region have sex determination and dosage compensation defects, and XO males with two doses are more severely affected and die. The hermaphrodite defects are suppressed by a downstream mutation that forces all animals into the XX mode of sex determination and dosage compensation. The male lethality is suppressed by mutations that force all animals into the XO mode of both processes. We were able to subdivide this region into three smaller regions, each of which contains at least one signal element. We propose that the X chromosome component of the sex-determination signal is the dose of a relatively small number of genes.

The conditioning connection

1990 ◽  
Vol 329 (1253) ◽  
pp. 179-186 ◽  
Keyword(s):  
Learning Rule ◽  
Connection Weight ◽  
The Past ◽  
Learning Rules ◽  
Signal Element ◽  
History Of ◽  
Stored Information

In 1948 Konorski argued that conditioning reflects the strengthening of a connection between elements representing the signal and the reinforcer, as a result of the coincidence of activity in the signal element with a rise in activity in the reinforcer element. This Konorskian process represents one way of implementing an error-correcting learning rule and thus, unlike a simple Hebbian process, anticipates selective conditioning, such as that observed in Kamin’s blocking procedure. However, the Konorskian process, in common with other error-correcting learning rules, fails to explain why blocking is attentuated by ‘surprising’ changes in reinforcement conditions that should not augment activity in the reinforcer element. Rather, the reinforcer-specificity of such unblocking suggests the operation of an associability process by which stored information about the past predictive history of the signal is expressed at the connection between signal and reinforcer elements to modulate changes in the connection weight.

scholarly journals Coding sequence composition flanking either signal element alters V(D)J recombination efficiency

1995 ◽  
Vol 23 (6) ◽  
pp. 1060-1067 ◽  
Author(s):  
Nikolai V. Boubnov ◽  
Zachary P. Wills ◽  
David T. Weaver
Keyword(s):  
Coding Sequence ◽  
Sequence Composition ◽  
Recombination Efficiency ◽  
Signal Element
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