A predicted membrane protein, TRA-2A, directs hermaphrodite development in Caenorhabditis elegans

Development ◽  
1995 ◽  
Vol 121 (9) ◽  
pp. 2995-3004 ◽  
Author(s):  
P.E. Kuwabara ◽  
J. Kimble
Keyword(s):  
Heat Shock ◽  
Membrane Protein ◽  
Cell Fate ◽  
Loss Of Function ◽  
Heat Shock Promoter ◽  
Somatic Development ◽  
C Elegans ◽  
Cellular Domain ◽  
Carboxy Terminal ◽  
Necessary And Sufficient

The nematode C. elegans naturally develops as either an XO male or XX hermaphrodite. The sex-determining gene, tra-2, promotes hermaphrodite development in XX animals. This gene encodes a predicted membrane protein, named TRA-2A, which has been proposed to provide the primary feminising activity of the tra-2 locus. Here, we show that transgenic TRA-2A driven from a heat shock promoter can fully feminise the somatic tissues of XX tra-2 loss-of-function mutants, which would otherwise develop as male. TRA-2A is thus likely to provide a component of the tra-2 locus that is both necessary and sufficient to promote female somatic development. Transgenic TRA-2A driven by the heat shock promoter can also transform XO animals from male to self-fertile hermaphrodite. This result establishes the role of tra-2 as a developmental switch that controls somatic sexual cell fate. We show that a carboxy-terminal region of TRA-2A, predicted to be intra-cellular, can partially feminise XX tra-2 loss-of-function mutants and XO tra-2(+) males. We suggest that this intra-cellular domain of TRA-2A promotes hermaphrodite development by negatively regulating the FEM proteins.

scholarly journals Identification of a heat shock promoter in the topA gene of Escherichia coli.

1990 ◽  
Vol 172 (12) ◽  
pp. 6871-6874 ◽  
Author(s):  
S A Lesley ◽  
S B Jovanovich ◽  
Y C Tse-Dinh ◽  
R R Burgess
Keyword(s):  
Escherichia Coli ◽  
Heat Shock ◽  
Heat Shock Promoter

scholarly journals P transposons controlled by the heat shock promoter.

1986 ◽  
Vol 6 (5) ◽  
pp. 1640-1649 ◽  
Author(s):  
H Steller ◽  
V Pirrotta
Keyword(s):  
Heat Shock ◽  
Germ Line ◽  
Fusion Gene ◽  
P Element ◽  
Translational Efficiency ◽  
Heat Shock Promoter ◽  
P Elements ◽  
Heat Shocks ◽  
Neomycin Resistance ◽  
Heat Shock Induction

We have transformed Drosophila melanogaster with modified P-element transposons, which express the transposase function from the heat-inducible hsp70 heat shock promoter. The Icarus transposon, which contains a direct hsp70-P fusion gene, behaved like a very active autonomous P element even before heat shock induction. Although heat shock led to abundant somatic transcription, transposition of the Icarus element was confined to germ line cells. To reduce the constitutive transposase activity observed for the Icarus element, we attenuated the translational efficiency of the transposase RNA by inserting the transposon 5 neomycin resistance gene between the hsp70 promoter and the P-element sequences. The resulting construct, called Icarus-neo, conferred resistance to G418, and its transposition was significantly stimulated by heat shock. Heat shocks applied during the embryonic or third instar larval stage had similar effects, indicating that transposition of P elements is not restricted to a certain developmental stage. Both Icarus and Icarus-neo destabilized snw in a P-cytotype background and thus at least partially overcome the repression of transposition. Our results suggest that the regulation of P-element transposition occurs at both the transcriptional and posttranscriptional levels.

scholarly journals Induction of dnaK through Its Native Heat Shock Promoter Is Necessary for Intramacrophagic Replication of Brucella suis

2002 ◽  
Vol 70 (3) ◽  
pp. 1631-1634 ◽  
Author(s):  
Stephan Köhler ◽  
Euloge Ekaza ◽  
Jean-Yves Paquet ◽  
Karl Walravens ◽  
Jacques Teyssier ◽  
...  
Keyword(s):  
Heat Shock ◽  
Mouse Model ◽  
High Sensitivity ◽  
Murine Macrophage ◽  
Null Mutant ◽  
Intracellular Replication ◽  
Heat Shock Promoter ◽  
Brucella Suis ◽  
Independent Synthesis ◽  
Mouse Model Of Infection

ABSTRACT The heat shock protein DnaK is essential for intramacrophagic replication of Brucella suis. The replacement of the stress-inducible, native dnaK promoter of B. suis by the promoter of the constitutively expressed bla gene resulted in temperature-independent synthesis of DnaK. In contrast to a dnaK null mutant, this strain grew at 37°C, with a thermal cutoff at 39°C. However, the constitutive dnaK mutant, which showed high sensitivity to H2O2-mediated stress, failed to multiply in murine macrophage-like cells and was rapidly eliminated in a mouse model of infection, adding strong arguments to our hypothesis that stress-mediated and heat shock promoter-dependent induction of dnaK is a crucial event in the intracellular replication of B. suis.

scholarly journals The DNA-binding activity of the human heat shock transcription factor is regulated in vivo by hsp70.

1993 ◽  
Vol 13 (9) ◽  
pp. 5427-5438 ◽  
Author(s):  
D D Mosser ◽  
J Duchaine ◽  
B Massie
Keyword(s):  
Transcription Factor ◽  
Heat Shock ◽  
Dna Binding ◽  
Elevated Temperatures ◽  
Active Role ◽  
Heat Shock Transcription Factor ◽  
Response To Treatment ◽  
Promoter Element ◽  
Heat Shock Promoter

The human heat shock transcription factor (HSF) is maintained in an inactive non-DNA-binding form under nonstress conditions and acquires the ability to bind specifically to the heat shock promoter element in response to elevated temperatures or other conditions that disrupt protein structure. Here we show that constitutive overexpression of the major inducible heat shock protein, hsp70, in transfected human cells reduces the extent of HSF activation after a heat stress. HSF activation was inhibited more strongly in clones that express higher levels of hsp70. These results demonstrate that HSF activity is negatively regulated in vivo by hsp70 and suggest that the cell might sense elevated temperature as a decreased availability of hsp70. HSF activation in response to treatment with sodium arsenite or the proline analog azetidine was also depressed in hsp70-expressing cells relative to that in the nontransfected control cells. As well, the level of activated HSF decreased more rapidly in the hsp70-expressing clones when the cells were heat shocked and returned to 37 degrees C. These results suggest that hsp70 could play an active role in the conversion of HSF back to a conformation that does not bind the heat shock promoter element during the attenuation of the heat shock response.

Regulation of insulin biosynthesis in non-beta cells by a heat shock promoter

2013 ◽  
Vol 116 (2) ◽  
pp. 147-151 ◽  
Author(s):  
Vahid Jajarmi ◽  
Mojgan Bandehpour ◽  
Bahram Kazemi
Keyword(s):  
Heat Shock ◽  
Beta Cells ◽  
Insulin Biosynthesis ◽  
Heat Shock Promoter

Rhodopsin maturation antagonized by dominant rhodopsin mutants

1998 ◽  
Vol 15 (4) ◽  
pp. 693-700 ◽  
Author(s):  
PHANI KURADA ◽  
TIMOTHY D. TONINI ◽  
MICHELLE A. SERIKAKU ◽  
JONATHAN P. PICCINI ◽  
JOSEPH E. O'TOUSA
Keyword(s):  
Heat Shock ◽  
Vitamin A ◽  
Visual Pigment ◽  
Gene Activation ◽  
Dominant Allele ◽  
Wild Type ◽  
Rhodopsin Gene ◽  
Heat Shock Promoter ◽  
Complex Forms

ninaED1, a dominant allele of the major Drosophila rhodopsin gene, expresses a rhodopsin that is predominantly recovered in a 80-kD complex that likely represents rhodopsin dimers. By driving either ninaED1 or ninaE+ expression from a heat-shock promoter, we show that the 80-kD rhodopsin complex forms immediately after gene activation. In wild type, but not ninaED1, rhodopsin monomeric forms are detected at later times. The generation of monomeric forms of wild-type rhodopsin is suppressed in vitamin A-deprived flies or in flies heterozygous for the dominant rhodopsin mutation. We also show that ninaED1 expression does not affect the maturation of another Drosophila visual pigment, Rh3. These results are consistent with the view that the ninaED1 rhodopsin antagonizes an early posttranslation process that is specific for maturation of the ninaE-encoded rhodopsin.

scholarly journals Transcription of Dictyostelium discoideum transposable element DIRS-1.

1984 ◽  
Vol 4 (11) ◽  
pp. 2332-2340 ◽  
Author(s):  
S M Cohen ◽  
J Cappello ◽  
H F Lodish
Keyword(s):  
Heat Shock ◽  
Transposable Element ◽  
Dictyostelium Discoideum ◽  
Cdna Clone ◽  
Terminal Repeat ◽  
Transcriptional Initiation ◽  
Heat Shock Promoter ◽  
Terminal Repeats ◽  
Discrete Site ◽  
The Right

DIRS-1 is a Dictyostelium discoideum transposable element that contains heat shock promoter sequences in the inverted terminal repeats. We showed that transcription of a 4.5-kilobase polyadenylated RNA initiates at a discrete site within the left-terminal repeat of DIRS-1, downstream from heat shock promoter and TATA box sequences. This RNA represents a full-length transcript of DIRS-1. We describe a cDNA clone that contains the 4.1 kilobases of internal sequence of DIRS-1, a cDNA clone that spans the junction between the internal sequences and the right-terminal repeat, and a cDNA clone that appears to have been transcribed from a rearranged genomic copy of DIRS-1. A second DIRS-1 RNA, named E1, is transcribed on the opposite strand of DIRS-1 from the 4.5-kilobase RNA and is under control of the heat shock promoter in the right-terminal repeat. E1 transcription initiates at multiple positions both within and downstream from the right-terminal repeat. The same transcriptional initiation sites are used during normal development and during heat shock, suggesting that in all cases DIRS-1 transcription is regulated by the heat shock promoters contained within the two terminal repeats.

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