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

Louise Sefton; John R. Timmer; Yan Zhang; Florence Béranger; Thomas W. Cline

doi:10.1038/35016119

The Primary Sex Determination Signal of Caenorhabditis elegans

Genetics ◽

10.1093/genetics/152.3.999 ◽

1999 ◽

Vol 152 (3) ◽

pp. 999-1015 ◽

Cited By ~ 3

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.

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

Genetics ◽

10.1093/genetics/138.4.1105 ◽

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.

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Sex determination

AccessScience ◽

10.1036/1097-8542.617400 ◽

2015 ◽

Keyword(s):

Sex Determination

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Sex determination banned in India

Nature ◽

10.1038/379201e0 ◽

1996 ◽

Vol 379 (6562) ◽

pp. 201-201

Keyword(s):

Sex Determination

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Inhibition of interferon alpha signalling through the Jak-STAT pathway in HCV transgenic mice

Journal of Hepatology ◽

10.1016/s0168-8278(01)80077-5 ◽

2001 ◽

Vol 34 (0) ◽

pp. 25-26

Author(s):

M Heim

Keyword(s):

Transgenic Mice ◽

Interferon Alpha ◽

Stat Pathway

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Role of JAK-STAT pathway in pulmonary fibrosis

Pneumologie ◽

10.1055/s-0033-1345044 ◽

2013 ◽

Vol 67 (05) ◽

Cited By ~ 2

Author(s):

J Eschenbrenner ◽

W Janssen ◽

B Kojonazarov ◽

K Murmann ◽

A Ghofrani ◽

...

Keyword(s):

Pulmonary Fibrosis ◽

Stat Pathway

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Sex determination and Y chromosome constitutive heterochromatin

Current Research in Biochemistry and Molecular Biology ◽

10.33702/crbmb.2019.1.1.1 ◽

2019 ◽

Vol 1 (1) ◽

pp. 1-5

Author(s):

Abyt Ibraimov

Keyword(s):

Sex Determination ◽

Y Chromosome ◽

Constitutive Heterochromatin ◽

Sex Differentiation ◽

Secondary Sexual Characteristics ◽

Biological Meaning ◽

Heterochromatin Block ◽

Sexual Characteristics ◽

Open Question ◽

Efficient Elimination

In many animals, including us, the genetic sex is determined at fertilization by sex chromosomes. Seemingly, the sex determination (SD) in human and animals is determined by the amount of constitutive heterochromatin on Y chromosome via cell thermoregulation. It is assumed the medulla and cortex tissue cells in the undifferentiated embryonic gonads (UEG) differ in vulnerability to the increase of the intracellular temperature. If the amount of the Y chromosome constitutive heterochromatin is enough for efficient elimination of heat difference between the nucleus and cytoplasm in rapidly growing UEG cells the medulla tissue survives. Otherwise it doomed to degeneration and a cortex tissue will remain in the UEG. Regardless of whether our assumption is true or not, it remains an open question why on Y chromosome there is a large constitutive heterochromatin block? What is its biological meaning? Does it relate to sex determination, sex differentiation and development of secondary sexual characteristics? If so, what is its mechanism: chemical or physical? There is no scientifically sound answer to these questions.

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