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Female specific genes

Hirai, H., Tanaka, M. and LoVerde, P.T. (1993) Schistosoma mansoni chromosomal localization of female-specific genes and a female-specific DNA element. Experimental Parasitology 76, 1 75-1 81. [Pg.73]

Crevelding, C.C., Sommer, C. and Kunz, W. (1997) Female-specific gene expression in Schistosoma mansorii is regulated by pairing. Parasitology 1 15, 635-640. [Pg.148]

Freebern, W.J., Osman, A., Niles, E.G., Christen, L. and LoVerde, P.T. (1999a) Identification of a cDNA encoding a retinoid X receptor homologue from Schistosoma mansoni. Evidence for a role in female-specific gene expression, journal of Biological Chemistry 274, 4577 t585. [Pg.224]

Fig. 11.4 Class I and class II sex-specific genes. Class I male-specific genes are induced by plasma growth hormone (GH) pulses in male liver (a) and class I female-specific genes are induced by the more continuous female plasma GH profile in female liver (b). Class II male-speeific genes are repressed in female liver by the female plasma GH profile (a) and class II female-specific genes are repressed in male liver by the male plasma GH profile (b). Consequently, the loss of GH following hypophysec-tomy ( hypox ) leads to downregulation of class I male-specific genes and to upregulation of class II female-spe-... Fig. 11.4 Class I and class II sex-specific genes. Class I male-specific genes are induced by plasma growth hormone (GH) pulses in male liver (a) and class I female-specific genes are induced by the more continuous female plasma GH profile in female liver (b). Class II male-speeific genes are repressed in female liver by the female plasma GH profile (a) and class II female-specific genes are repressed in male liver by the male plasma GH profile (b). Consequently, the loss of GH following hypophysec-tomy ( hypox ) leads to downregulation of class I male-specific genes and to upregulation of class II female-spe-...
Embryonic stem (ES) cells selected in this manner are placed into a pseudopregnant female. The first generation litter (El) should have one normal and one mutated copy of the gene. If one then crosses the FI generation, one-quarter of the next generation will have two copies of the knocked-out gene. These animals can now be examined for any phenotype that results from the absence of that specific gene. [Pg.79]

Figure 9.4 Simplified view of the genetic cascade regulating sexual development in D. melanogaster. Genes are in italics, proteins in upper case. The ratio of X chromosomes to autosomes determines whether Sxl is activated. SXL acts as a splicing factor on the RNA produced by tra, resulting in the production of active TRA protein in females, inactive in males. TRA (together with TRA-2) determines the female-specific splicing of fru, dsf and dsx. Figure 9.4 Simplified view of the genetic cascade regulating sexual development in D. melanogaster. Genes are in italics, proteins in upper case. The ratio of X chromosomes to autosomes determines whether Sxl is activated. SXL acts as a splicing factor on the RNA produced by tra, resulting in the production of active TRA protein in females, inactive in males. TRA (together with TRA-2) determines the female-specific splicing of fru, dsf and dsx.
Chertemps, T., Duportets, L., Labeur, C., Ueyama, M. and Wicker-Thomas, C. (2006). A female-specific desaturase gene responsible for diene hydrocarbon biosynthesis and courtship behaviour in Drosophila melanogaster. Insect Mol. Biol., 15,465—473. Chertemps, T., Duportets, L., Labeur, C. and Wicker-Thomas, C. (2005). A new elongase selectively expressed in Drosophila male reproductive system. Biochem. Biophys. Res. Commun., 333,1066-1072. [Pg.70]

A female-specific desaturase gene responsible for diene hydrocarbon biosynthesis and courtship behaviour in Drosophila melanogaster. Insect Mol. Biol., 15,465 473. [Pg.151]

Mogil JS, Wilson SG, Chesler EJ, et al. The melanocortin-1 receptor gene mediates female-specific mechanisms of analgesia in mice and humans. Proc Natl Acad Sci U S A 2003 100(8) 4867-72. [Pg.94]

By reversing the polarity of the DNA strands, the opposite strand will be transcribed and a complementary or antisense RNA will be produced. When antisense RNA was introduced either in vitro (27) or in vivo (28), the presence of the antisense RNA inhibited the expression of the normal RNA transcript produced by the resident gene. Suppression of RNA translation by antisense RNA may be due to the formation of an RNA heteroduplex between the two complementary RNA strands thus blocking the attachment of ribosomes. An example of this application in the context of the Adh example would be the construction of a chimeric gene containing the antisense sequence for Adh linked with a female-specific promoter. Thus, Adh activity would be eliminated from females and make them lethally sensitive to treatment with ethanol. [Pg.141]

The Sxl protein, encoded by the sex-lethal gene, is the first protein to act in the cascade. Early in development, this gene is transcribed from a promoter that functions only in female embryos. Later in development, this female-specific promoter is shut off and another promoter for sex lethal becomes active in both male and female embryos. However, in the absence of early Sxl protein, the sex-lethal pre-mRNA in male embryos is spliced to produce an mRNA that contains a stop codon early in the sequence. The net result is that male embryos produce no functional Sxl protein either early or later in development. [Pg.505]


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