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PubMed2004

Molecular complexity of sexual development and gene regulation in Plasmodium falciparum.

The malaria parasite, Plasmodium falciparum, has a complex life cycle which alternates between the vertebrate host and the invertebrate vector. Various morphological changes as well as stage-specific transcripts and gene expression profiles that accompany parasite's asexual and sexual life cycle suggest that gene regulation is crucial for the parasite's continual adaptations to survive the changing environments as well as for pathogenesis. Development of sexual stages is crucial for malaria transmission and relatively little is known about the role of specific gene products during asexual to sexual differentiation and further development. Therefore, in order to have a full understanding of the biology of the malaria parasite, gene regulation on a genome-wide global level must be understood, an area remaining to be elucidated in P. falciparum. Parasite features, such as A-T bias, difficulties in cloning, labor-intensive culture and purification of specific stages of the parasite, all contribute to the difficulties to investigate many aspects of parasite biology. However, despite these challenges, limited studies have revealed a number of parallelisms with eukaryotic transcription. For example, the parasite's genes are organised in a similar fashion, contain promoter elements and upstream activation sequences, as shown by structural searches and functional assays, and some of the basal machinery and general transcription factors have been found in Plasmodium. The completion of the full genome sequence of P. falciparum and other species of Plasmodium has resulted in the search for specific transcription factors through genome mining. Although genome mining may identify some of the factors, search for these factors solely by primary sequence homology would result in a non-comprehensive list for transcription factors present in the genome. Here, we present further discussion on putative transcription factors like activities detected in the asexual and sexual stages of P. falciparum.

Animals↗
PubMed1992

[A body of one's own. Sexual development and physical female development in the mother-child relationship].

Prevalent psychoanalytic opinion has it that (sexually) femaleness is marked by a severe deficiency. Accordingly it is widely held that the acknowledgement of female sexuality is primarily a matter for fathers rather than mothers. The author takes a different stance, insisting on the opportunities inherent in the mother-daughter relationship to the extent that it both permits and encourages pleasurable self-examination and acceptance of the body on the part of the growing girl. In the therapeutic connection, the author calls for a form of remedial socialisation to fill the specific lacunae that have developed around female sexuality.

Body Image↗
PubMed2002

Anomalies of human sexual development: clinical aspects and genetic analysis.

Disorders of human sex determination result in malformations of the external and internal genitalia. These malformations may vary from sexual ambiguity to complete sex reversal (XY female, XX male). Most of the knowledge of the molecular mechanisms involved in the mammalian sex determination pathway has been derived from the genetic analysis of intersex patients. Clinical management of these conditions critically depends on a precise understanding of their pathophysiology. Until recently, only transcription factors such as SRY, SOX9, DAX1, WT1 and SF1 were known to be responsible for abnormal gonadal development and sexual ambiguity. Gonadal dysgenesis may be isolated, as in the case of SRY mutations, or associated with abnormal development of other organs, such as bone or adrenals, consistent with the spatial expression profile of the disrupted genes (SOX9 or SF1). WNT4 is a new sex-determining signalling molecule. Deletions of Wnt4 were shown to be responsible for the masculinization of XX mouse pups while its duplication and overexpression in humans leads to XY sex reversal. Similarly, duplications of loci containing DAX1 or SOX9 have also been shown to cause sex reversal. These results support the emerging concept that mammalian sex determination is dosage sensitive at multiple steps of its pathway.

Aging↗
PubMed2005

Somatic control of germline sexual development is mediated by the JAK/STAT pathway.

Germ cells must develop along distinct male or female paths to produce the sperm or eggs required for sexual reproduction. In both mouse and Drosophila, the sexual identity of germ cells is influenced by the sex of the surrounding somatic tissue (for example, refs 1, 2, reviewed in refs 3, 4); however, little is known about how the soma controls germline sex determination. Here we show that the janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway provides a sex-specific signal from the soma to the germ line in Drosophila embryonic gonads. The somatic gonad expresses a JAK/STAT ligand, unpaired (upd), in a male-specific manner, and activates the JAK/STAT pathway in male germ cells at the time of gonad formation. Furthermore, the JAK/STAT pathway is necessary for male-specific germ cell behaviour during early gonad development, and is sufficient to activate aspects of male germ cell behaviour in female germ cells. Our findings provide direct evidence that the JAK/STAT pathway mediates a key signal from the somatic gonad that regulates male germline sexual development.

Animals↗