Magnesium (Mg2+) plays an essential role in many biological processes. Mg2+ deficiency is therefore associated with a wide range of clinical effects including muscle cramps, fatigue, seizures and arrhythmias. To maintain sufficient Mg2+ levels, (re)absorption of Mg2+ in the intestine and kidney is tightly regulated. Genetic defects that disturb Mg2+ uptake pathways, as well as drugs interfering with Mg2+ (re)absorption cause hypomagnesemia. The aim of this review is to provide an overview of the molecular mechanisms underlying genetic and drug-induced Mg2+ deficiencies. This leads to the identification of four main mechanisms that are affected by hypomagnesemia-causing mutations or drugs: luminal transient receptor potential melastatin type 6/7-mediated Mg2+ uptake, paracellular Mg2+ reabsorption in the thick ascending limb of Henle's loop, structural integrity of the distal convoluted tubule and Na+-dependent Mg2+ extrusion driven by the Na+/K+-ATPase. Our analysis demonstrates that genetic and drug-induced causes of hypomagnesemia share common molecular mechanisms. Targeting these shared pathways can lead to novel treatment options for patients with hypomagnesemia.

Ovarian stimulation with exogenous follicle stimulating hormone (FSH) has been used to increase the number of viable oocytes for laparoscopic oocyte recovery (LOR) in goats. The aim of this study was to evaluate the effect of two FSH protocols for ovarian stimulation in goats on the expression pattern of epidermal growth factor (EGF) receptor (EGFR) in cumulus–oocyte complexes (COCs) recovered by LOR. After real-time qRT-PCR analysis, expression profiles of morphologically graded COCs were compared prior to and after in vitro maturation (IVM) on a FSH protocol basis. The use of a protocol with higher number of FSH injections at a shorter interval resulted in GI/GII COCs with a higher level of EGFR expression in cumulus cells, but not in the oocyte, which was correlated with an elevated meiotic competence following IVM. Based on the maturation profile and EGFR expression patterns observed between groups, the morphological selection of COCs prior to IVM was not a good predictor of oocyte meiotic competence. Therefore, EGFR may be a good candidate marker for indirect prediction of goat oocyte quality. The IVM process of goat COCs increased the EGFR expression in oocytes and cumulus cells, which seemed to be strongly associated with the resumption of meiosis. In summary, differential EGFR expression in goat cumulus cells was associated with the in vivo prematuration process, and in turn, the upregulation in the entire COC was associated with IVM. Cause-and-effect relationships between such increased expression levels, particularly in the oocyte, and oocyte competence itself still need to be further investigated.

To examine the possibility that epidermal growth factor (EGF) and its receptor (EGF-R) are expressed throughout folliculogenesis, we studied the presence and distribution of EGF and EGF-R in goat ovaries. Ovaries of goats were collected and either fixed in paraformaldehyde for immunohistochemical localization of proteins, or used for the isolation of follicles, luteal cells and ovarian surface epithelium to study mRNA expression for EGF and EGF-R, using the reverse transcriptase polymerase chain reaction. EGF protein and mRNA were found in primordial, primary and secondary follicles as well as in small and large antral follicles and in surface epithelium, but in corpora lutea only the protein could be detected. Antral follicles expressed EGF mRNA in oocyte, cumulus, mural granulosa and theca cells. For EGF-R, both protein and mRNA were present at all stages of follicular development and in all antral follicular compartments. EGF-R protein and mRNA were also found in corpora lutea and surface epithelium. It is concluded that EGF and its receptor are expressed in goat ovarian follicles at all stages of follicle development, in corpora lutea, and in ovarian surface epithelium.

During insect development, morphological differences between segments are controlled by the Hox gene family of transcription factors. Recent evidence also suggests that variation in the regulatory elements of these genes and their downstream targets underlies the evolution of several segment-specific morphological traits. This review introduces a new model system, the larval oenocyte, for studying the evolution of fate specification by Hox genes at single-cell resolution. Oenocytes are found in a wide range of insects, including species using both the short and the long germ modes of development. Recent progress in our understanding of the genetics and cell biology of oenocyte development in the fruitfly Drosophila melanogaster is discussed. In the D. melanogaster embryo, the formation of this cell type is restricted to the first 7 abdominal segments and is under Hox gene control. Oenocytes delaminate from the dorsal ectoderm of A1-A7 in response to an induction that involves the epidermal growth factor receptor (EGFR) signalling pathway. Although the receptor itself is required in the presumptive oenocytes, its ligand Spitz (Spi) is secreted by a neighbouring chordotonal organ precursor (COP). Thus, in dorsal regions, local signalling from this component of the developing peripheral nervous system induces the formation of oenocytes. In contrast, in lateral regions of the ectoderm, Spi signal from a different COP induces the formation of secondary COPs in a homeogenetic manner. This dorsoventral difference in the fate induced by Spi ligand is controlled by a prepattern in the responding ectoderm that requires the Spalt (Sal) transcription factor. Sal protein is expressed in the dorsal but not lateral ectoderm and acts as a competence modifier to bias the response to Spi ligand in favour of the oenocyte fate. We discuss a recently proposed model that integrates the roles of Sal and the EGFR pathway in oenocyte/chordotonal organ induction. This model should provide a useful starting point for future comparative studies of these ectodermal derivatives in other insects.