The root meristem is shaped by brassinosteroid control of cell geometry

Growth extent and direction determine cell and whole-organ architecture. How they are spatio-temporally modulated to control size and shape is not well known. Here we tackled this question by studying the effect of brassinosteroid (BR) signalling on the structure of the root meristem. Quantification of the three-dimensional geometry of thousands of individual meristematic cells across different tissue types showed that the modulation of BR signalling yields distinct changes in growth rate and anisotropy, which affects the time that cells spend in the meristem and has a strong impact on the final root form. By contrast, the hormone effect on cell volume was minor, establishing cell volume as invariant to the effect of BR. Thus, BR has the highest effect on cell shape and growth anisotropy, regulating the overall longitudinal and radial growth of the meristem, while maintaining a coherent distribution of cell sizes. Moving from single-cell quantification to the whole organ, we developed a computational model of radial growth. The simulation demonstrates how differential BR-regulated growth between the inner and outer tissues shapes the meristem and thus explains the non-intuitive outcomes of tissue-specific perturbation of BR signalling. The combined experimental data and simulation suggest that the inner and outer tissues have distinct but coordinated roles in growth regulation.

Thyroid Hormone Effect on the Differentiation of Human Induced Pluripotent Stem Cells into Hepatocyte-Like Cells

Human induced pluripotent stem cells (hiPSCs) hold great potential as an unlimited source for obtaining hepatocyte-like cells (HLCs) for drug research. However, current applications of HLCs have been severely limited by the inability to produce mature hepatocytes from hiPSCs in vitro. Thyroid hormones are one of the hormones that surge during the perinatal period when liver maturation takes place. Here we assessed the influence of thyroid hormone on hepatic progenitor differentiation to HLCs. We analyzed gene and protein expression of early and late hepatic markers and demonstrated the selective activity of thyroid hormone on different genes. Particularly, we demonstrated thyroid hormone-dependent inhibition of the fetal hepatic marker AFP. Our study sheds light on the role of thyroid hormone during liver differentiation and maturation.

Glyphosate in the production and forage quality of marandu grass

The drift of the herbicide glyphosate, used for desiccating crops or controlling weeds, can result in growth-promoting or non-target plant development effects. Thus, it is possible to use the compound to increase the biomass of forage through the hormone effect. The objective of this study was to evaluate the effects of sublethal doses of glyphosate on the production of Urochloa brizantha cv. Marandu (Marandu grass) and its nutritional quality in ruminants. The design used was completely randomized, with five replications in a factorial scheme. The treatments used were as follows: control (without glyphosate application) and four sublethal doses of glyphosate (4, 10, 14, and 20 g ha-1 of the acid equivalent). The monthly collections consisted of collecting the plant material (0.20 m) from the surface, comprising of leaves and pseudocolmos (stem and leaf sheath) to determine the dry matter production and forage chemical-bromatological parameters. The results showed that leaf/stem ratio, neutral detergent fiber, and acid detergent fiber were affected exclusively by the harvest factor. The hormone effect of the herbicide occurs in the production of dry matter and lignin in the evaluated subdoses. For crude protein, there was an interaction between the factor doses and harvest, due to the effect of glyphosate and the management applied to the harvests, showing that the sublethal doses of glyphosate promoted the production of dry matter and the food quality of Marandu grass.

Root meristem shaping via brassinosteroid-controlled cell geometry

Growth extent and direction determine cell and whole-organ architecture. How they are spatiotemporally modulated to control size and shape? Here we tackled this question by studying the effect of brassinosteroid (BR) signaling on the structure of the root meristem. Quantification of the 3D geometry of thousands of individual meristematic cells across different tissue types showed that modulation of BR signaling yields distinct changes in growth rate and anisotropy, which affects the time cells spend in the meristem and has a strong impact on final root form. By contrast, the hormone effect on cell volume was minor, establishing cell volume as invariant to the effect of BR. Thus, BR has highest effect on cell shape and growth anisotropy, regulating overall radial growth of the meristem, while maintaining a coherent distribution of cell sizes. Moving from single-cell quantification to the whole organ, we developed a computational model of radial growth that demonstrates how differential growth regulation by BR between the inner and outer tissues shapes the meristem. The model explains the unintuitive outcomes of tissue-specific perturbation of BR signaling and suggests that the inner and outer tissues have independent but coordinated roles in growth regulation.

Luteinizing Hormone Effect on Luteal Cells Is Dependent on the Corpus Luteum Stage in Felids

The objective of this study was to investigate the effect of luteinizing hormone (LH) on steroidogenic luteal cells obtained from corpora lutea (CL) of the domestic cat and selected wild felids. Luteal cells were isolated enzymatically from CL at different developmental stages and cultured for two days in the presence and absence of 100 ng/mL LH, respectively. Functionality was assessed by progesterone (P4) accumulation in cell culture media determined by ELISA. In addition, steroidogenic function was confirmed using immunohistochemistry for 3β-hydroxysteroid dehydrogenase (HSD3B). The enzymatic method allowed for the isolation of mostly small luteal cells in all investigated felids. Treatment with LH resulted in an increase in P4 secretion of cultured luteal cells obtained from CL in the formation stage (African lion) and development/maintenance stage (domestic cat (p < 0.05), Javan leopard), whereas luteal cells from more advanced stages of luteal development (regression) responded moderately or not at all to LH stimulation (domestic cat, Asiatic golden cat, Asiatic lion). The protein signal for HSD3B on CL was visible until development/maintenance. In conclusion, this study shows that LH promotes P4 production in luteal cells only until the onset of regression, when morphological signs are visible on the CL of felids and HSD3B is no longer detectable.

Evidence of growth hormone effect on plasma leptin in diet-induced obesity and diet-resistant rats

Background Plasma leptin is regulated by several factors, including growth hormone (GH), which influences the pathophysiology of obesity. Objective To demonstrate the short-term effect of GH on plasma leptin levels in 3 conditions in vivo with the different amount of body fat mass. Methods Adult male Wistar rats were fed with standard chow or hypercaloric diet (HC). The HC rats were demonstrated as HC-feeding obese (HC-O) and HC-feeding resistant (HC-R) rats. Then, they were treated with GH or saline for 3 days. Basal plasma leptin levels were measured at 24 and 32 h. For meal-induced condition, all rats were fed for 2 hand plasma leptin was measured. Further 16-h fasting period, plasma leptin, insulin, and insulin sensitivity indexes were determined. Results The short-term GH treatment decreased basal plasma leptin at 32 h after the first GH injection in HC-O rats. However, GH treatment had no effect on meal-induced plasma leptin in all rats. Furthermore, GH treatment attenuated fasting effect on plasma leptin in control and HC-R rats. The insulin resistance (IR) induced by the short-term GH treatment was demonstrated by higher fasting plasma insulin and the increased homeostasis model of IR in HC-R rats. Conclusions The study demonstrates the important role of greater fat mass in HC-O rats, which results in decreased basal plasma leptin after short-term GH treatment. For meal-induced condition, GH had no effect on plasma leptin in all rats. Interestingly, GH could attenuate fasting effect on plasma leptin in rats that have lower fat mass.