Genetic Studies in Advanced Sugarcane Mid-Late Clones through Yield and Quality Traits

Sugarcane varietal development is frequently aimed at increasing yield and sucrose quality. Effective crop genetic evolution requires knowledge of the numerous traits that contribute to the present diversity by genetic analysis. Keeping in view, this experiment was conducted using a randomized block design with three replications and the trial consisted of nine mid-late sugarcane genotypes. Data on cane yield and quality traits were used to estimate the genetic variability parameters, heritability, and genetic advance (GA). Analysis of variance revealed highly significant and significant differences for all studied traits. Evaluated characters exhibited different levels of variability, heritability, and genetic advance among the studied genotypes. Low to high phenotypic coefficient of variation (PCV) and genotypic coefficient of variation (GCV) were recorded. The moderate GCV and PCV values were found particularly for Sugar Yield at harvest (18.09% and 21.64%) and Cane Yield at harvest (16.62% and 20.14%) respectively, whereas the lowest GCV and PCV (1.43% and 2.26% respectively) manifested for Purity at the 12 months stage. The highest broad sense heritability value manifested for Pol in juice at 12 months stage (%) (86.47%) followed by CCS at 12 months stage (%) (85.43%), while the lowest heritability (35.00%) revealed only for Germination % at 30 DAP. In the present study, high heritability and genetic advance as a percentage of the mean (>50) was recorded for Millable canes at harvest (000/ha) and single cane weight at harvest (kg) indicating a predominance of additive gene action for these characters. Therefore the result of this study suggests the existence of variability for cane yield and quality traits in these sugarcane genotypes, which should be exploited in future breeding

11β-hydroxysteroid dehydrogenase type 1 within osteoclasts mediates the bone protective properties of therapeutic corticosteroids in chronic inflammation

Therapeutic glucocorticoids (GCs) are powerful anti-inflammatory tools in the management of chronic inflammatory diseases such as rheumatoid arthritis (RA). However, their actions on bone in this context are complex. The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) is a mediator of the anti-inflammatory actions of therapeutic glucocorticoids (GCs) in vivo. In this study we delineate the role of 11β-HSD1 in the effects of GC on bone during inflammatory polyarthritis. Its function was assessed in bone biopsies from patients with RA and osteoarthritis, and in primary osteoblasts and osteoclasts. Bone metabolism was assessed in the TNF-tg model of polyarthritis treated with oral GC (corticosterone), in animals with global (TNF-tg(11βKO)), mesenchymal (including osteoblast) (TNF-tg(11βflx/tw2cre)) and myeloid (including osteoclast) (TNF-tg(11βflx/LysMcre)) deletion. Bone parameters were assessed by micro-CT, static histomorphometry and serum metabolism markers. We observed a marked increase in 11β-HSD1 activity in bone in RA relative to osteoarthritis bone, whilst the pro-inflammatory cytokine TNFα upregulated 11β-HSD1 within osteoblasts and osteoclasts. In osteoclasts, 11β-HSD1 mediated the suppression of bone resorption by GCs. Whilst corticosterone prevented the inflammatory loss of trabecular bone in TNF-tg animals, counterparts with global deletion of 11β-HSD1 were resistant to these protective actions, characterised by increased osteoclastic bone resorption. Targeted deletion of 11β-HSD1 within osteoclasts and myeloid derived cells partially reproduced the GC resistant phenotype. These data reveal the critical role of 11β-HSD1 within bone and osteoclasts in mediating the suppression of inflammatory bone loss in response to therapeutic GCs in chronic inflammatory disease