Conflicting language ideologies and contradictory language practices in Singaporean bilingual families

Informed by family language policy (FLP) as the theoretical framework, I illustrate in this paper how language ideologies can be incongruous and language policies can be conflicting through three multilingual families in Singapore representing three major ethnic groups – Chinese, Malay and Indian. By studying their family language audits, observing their language practices, and engaging in conversations about their language ideologies, I look at what these families do and do not do and what they claim to do and not to do. Data were collected over a period of 6 months with more than 700 minutes of recording of actual interactions. Analysis of the data reveals that language ideologies are ‘power-inflected’ and tend to become the source of educational and social tensions which in turn shape family language practices. In Singapore these tensions are illustrated by the bilingual policy recognising mother tongues (MTs) and English as official languages, and its educational policy establishing English as the medium of instruction. The view of English as having instrumental values and MTs as having cultural functions reveals that language choices and practices in family domains are value-laden in everyday interactions and explicitly negotiated and established through FLP.

Estrogen regulation of chicken riboflavin carrier protein gene is mediated by ERE half sites without direct binding of estrogen receptor

Estrogen is an important steroid hormone that mediates most of its effects on regulation of gene expression by binding to intracellular receptors. The consensus estrogen response element (ERE) is a 13 bp palindromic inverted repeat with a three nucleotide spacer. However, several reports suggest that many estrogen target genes are regulated by diverse elements, such as imperfect EREs and ERE half sites (ERE 1/2), which are either the proximal or the distal half of the palindrome. To gain more insight into ERE half site-mediated gene regulation, we used a region from the estrogen-regulated chicken riboflavin carrier protein (RCP) gene promoter that contains ERE half sites. Using moxestrol, an analogue of estrogen and transient transfection of deletion and mutation containing RCP promoter/reporter constructs in chicken hepatoma (LMH2A) cells, we identified an estrogen response unit (ERU) composed of two consensus ERE 1/2 sites and one non-consensus ERE 1/2 site. Mutation of any of these sites within this ERU abolishes moxestrol response. Further, the ERU is able to confer moxestrol responsiveness to a heterologous promoter. Interestingly, RCP promoter is regulated by moxestrol in estrogen responsive human MCF-7 cells, but not in other cell lines such as NIH3T3 and HepG2 despite estrogen receptor-alpha (ER-�) co transfection. Electrophoretic mobility shift assays (EMSAs) with promoter regions encompassing the half sites and nuclear extracts from LMH2A cells show the presence of a moxestrol-induced complex that is abolished by a polyclonal anti-ER� antibody. Surprisingly, estrogen receptor cannot bind to these promoter elements in isolation. Thus, there appears to be a definite requirement for some other factor(s) in addition to estrogen receptor, for the generation of a suitable response of this promoter to estrogen. Our studies therefore suggest a novel mechanism of gene regulation by estrogen, involving ERE half sites without direct binding of ER to the cognate elements.