No abstract

Crimp, a distinguishing feature of sheep fibres, significantly affects wool value, processing and final fabric attributes. Several explanations for fibre bending have been proposed. Most concentrate on relative differences in the physicochemical properties of the cortical cells, which comprise the bulk of the fibre. However, the associations between cortical properties and fibre crimp are not consistent and may not reflect the underlying causation of fibre curvature (FC). We have formulated a mechanistic model in which fibre shape is dictated primarily by the degree of asymmetry in cell supply from the follicle bulb, and the point at which keratinisation is completed within the follicle. If this hypothesis is correct, one would anticipate that most variations in fibre crimp would be accounted for by quantitative differences in both the degree of mitotic asymmetry in follicle bulbs and the distance from the bulb to the point at which keratinisation is completed. To test this hypothesis, we took skin biopsies from Merino sheep from sites producing wool differing widely in fibre crimp frequency and FC. Mitotic asymmetry in follicle bulbs was measured using a DNA-labelling technique and the site of final keratinisation was defined by picric acid staining of the fibre. The proportion of parato ortho-cortical cell area was determined in the cross-sections of fibres within biopsy samples. Mitotic asymmetry in the follicle bulb accounted for 0.64 ( P , 0.0001) of the total variance in objectively measured FC, while the point of final keratinisation of the fibre accounted for an additional 0.05 ( P , 0.05) of the variance. There was no association between ortho-to para-cortical cell ratio and FC. FC was positively associated with a subjective follicle curvature score ( P , 0.01). We conclude that fibre crimp is caused predominantly by asymmetric cell division in follicles that are highly curved. Differential pressures exerted by the subsequent asymmetric cell supply and cell hardening in the lower follicle cause fibre bending. The extent of bending is then modulated by the point at which keratinisation is completed; later hardening means the fibre remains pliable for longer, thereby reducing the pressure differential and reducing fibre bending. This means that even highly asymmetric follicles may produce a straight fibre if keratinisation is sufficiently delayed, as is the case in deficiencies of zinc and copper, or when keratinisation is perturbed by transgenesis. The model presented here can account for the many variations in fibre shape found in mammals.

Maternal diabetes and obesity are characterised by elevated blood glucose, insulin and lipids, resulting in upregulation of specific fuel-sensing and stress signalling pathways. Previously, we demonstrated that, separately, upregulation of the hexosamine biosynthetic pathway (HBP; under hyperglycaemic conditions) and endoplasmic reticulum (ER) stress (due to hyperlipidaemia) pathways reduce blastocyst development and alter oocyte metabolism. In order to begin to understand how both glucose and lipid metabolic disruptions influence oocyte developmental competence, in the present study we exposed mouse cumulus–oocyte complexes to hyperglycaemia (30 mM) and/or lipid (40 μM) and examined the effects on embryo development. The presence of glucosamine (GlcN; a hyperglycaemic mimetic) or increased lipid during in vitro maturation severely perturbed blastocyst development (P < 0.05). Hyperglycaemia, GlcN and hyperglycaemia + lipid treatments significantly increased HBP activity, increasing total O-linked glycosylation (O-GlcNAcylation) of proteins (P < 0.0001). All treatments also induced ER stress pathways, indicated by the expression of specific ER stress genes. The expression of genes encoding the HBP enzymes glutamine:fructose-6-phosphate amidotransferase 2 (Gfpt2) and O-linked β-N-acetylglucosaminyltransferase (Ogt) was repressed following lipid treatment (P < 0.001). These findings partially implicate the mechanism of O-GlcNAcylation and ER stress as likely contributors to compromised fertility of obese women.

The economically important characteristics of the adult fleece of Merino sheep, such as increases in clean fleece weight, fibre length, fibre diameter and crimp characteristics are determined during critical phases of fetal development of the skin and its appendages. Genetics plays a major role in the development of traits, but the maternal uterine environment could also influence development. Treatment of pregnant ewes with cortisol and its analogues has previously been shown to produce changes in wool follicle morphology. The aim of this study was to determine the effect of transient manipulation of maternal cortisol status during critical phases of wool follicle initiation and development in utero. From Days 55–65 post-conception, singleton-bearing Merino ewes were treated with metyrapone (cortisol inhibitor) or betamethasone (cortisol analogue). Lambs exposed to metyrapone in utero were born with hairier birthcoats than the control or betamethasone treatment groups (P < 0.05), displayed a 10% increase in staple length and a reduction in crimp frequency for the first three shearings (P < 0.05). Co-expression network analysis of microarray data revealed up-regulation of members of the transforming growth factor-β and chemokine receptor superfamilies, gene families known to influence hair and skin development. These experiments demonstrate that presumptive transient manipulation of maternal cortisol status coinciding with the initiation of fetal wool follicle development results in long-term alteration in fleece characteristics, namely fibre length and fibre crimp frequency. These results indicate it is possible to alter the lifetime wool production of Merino sheep with therapeutics targeted to gene expression during key windows of development in utero.