Eleven years of sexual discovery

A report on Novartis Foundation Symposium 244 "The Genetics and Biology of Sex Determination", London, UK, 1-3 May 2001.     

Eleven urgent questions of anxiety neurobiology

The author outlines in general and comments on urgent problems of the neurobiological basis of anxiety and corresponding experimental objectives.     

Eleven undescribedArizona serotypes isolated from man

Summary Eleven newArizona serotypes (1,3∶17, 20; 9∶1, 2, 10; 9∶1, 2, 36; 10∶1, 2, 36; 12∶23∶28; 14∶1, 2, 6; 18∶1, 3, 11; 19∶16, 17, 18; 20∶23∶21; 22∶13, 14; and 24∶24∶31) are described. With the exception of two strains (18∶1, 3, 11 and 24∶24∶31) isolated from the feces of asymptomatic persons, the organisms were derived from definite episodes of enteric, focal, or generalized infections. Types 1,3∶17, 20 and 10∶1, 2, 36 were isolated from blood cultures and type 22∶13, 14 from the blood, spinal fluid, and cerebral abscesses in a fatal case of meningoencephalitis.     

Attractive males do not sire superior daughters

Much of the recent work on the evolution of female choice has focused on the relative influence of direct and indirect benefits, and particularly whether direct costs can be offset by indirect benefits. Studies investigating whether attractive males benefit females by increasing the viability of their offspring often report mating advantages to sons consistent with the Fisher process, while detecting no or weak viability benefits. One potential reason for this is that sons may trade-off viability benefits with investment in costly traits that enhance mating success, leading to the suggestion that viability benefits may be better detected by examining daughters’ fitness. Here we investigate the relationship between male attractiveness and daughters’ fitness in Drosophila simulans. We measured daughter (and dam) lifetime reproductive success and longevity. We found no evidence that attractive males sire high fitness daughters. Additionally, neither daughters nor dams gained direct benefits from mating with attractive males. However, aspects of daughters’ fitness were related to dam characters.     

Preferential parental investment in daughters over sons

Female-biased parental investment is unusual but not unknown in human societies. Relevant explanatory models include Fisher’s principle, the Trivers-Willard model, local mate and resource competition and enhancement, and economic rational actor models. Possible evidence of female-biased parental investment includes sex ratios, mortality rates, parents’ stated preferences for offspring of one sex, and direct and indirect measurements of actual parental behavior. Possible examples of female-biased parental investment include the Mukogodo of Kenya, the Ifalukese of Micronesia, the Cheyenne of North America, the Herero of southern Africa, the Kanjar of south Asia, the Mundugumor of New Guinea, contemporary North America, and historical Germany, Portugal, and the United States. Lee Cronk is Assistant Professor of Anthropology at Texas A&M University, College Station, Texas. His main research interests are in human behavioral ecology, reproductive strategies, and East African hunter-gatherers and pastoralists.     

Evolution of the NANOG pseudogene family in the human and chimpanzee genomes

Background  

The NANOG gene is expressed in mammalian embryonic stem cells where it maintains cellular pluripotency. An unusually large family of pseudogenes arose from it with one unprocessed and ten processed pseudogenes in the human genome. This article compares the NANOG gene and its pseudogenes in the human and chimpanzee genomes and derives an evolutionary history of this pseudogene family.     

AMPK Promotes SPOP-Mediated NANOG Degradation to Regulate Prostate Cancer Cell Stemness

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TGFbeta and SMADs talk to NANOG in human embryonic stem cells

The TGFbeta/activin signaling pathway is important for the maintenance of human embryonic stem cells. In this issue of Cell Stem Cell, Xu et al. (2008) show that this pathway upregulates the expression of a key pluripotency gene NANOG through SMAD2/3.