Ecdysteroid juvenile hormone

The ecdysteroid dependence of developmental events during the larval-pupal transformation of the tobacco hornworm, Manduca sexta, was studied using the technique of abdomen ligation to eliminate the ecdysteroid-secreting prothoracic glands (PTG) in the thorax. The time at which a particular developmental event no longer required the presence of the PTG for its successful completion, ., when the event became ecdysteroid independent, was determined for the dendritic regression and death of proleg motor neuron PPR, the degeneration of its target muscle PPRM, and the secretion of pupal cuticle by the abdominal epidermis. Groups of abdomens were ligated from synchronously developing larvae at 12-hr intervals over the 4-day period preceding entry into the pupal stage. PPR's dendritic regression became ecdysteroid independent over the first 24 hr of this period. When abdomens were ligated midway through this period PPR became arrested in a partially regressed state. Twelve hours after PPR's regression became independent, the degeneration of PPRM and the secretion of pupal cuticle by the epidermis acquired independence. Another 12 hr elapsed before PPR's programmed death became independent. Thus, different developmental events acquired ecdysteroid independence in a stereotyped temporal sequence, and even different events within a single cell, ., PPR's regression and death, became independent at different times.

Nile red determination . The Nile red stock solution was prepared in acetone and stored protected from light following Tingaud-Sequeira et al. (2011) . Just before use, the working solution was prepared by diluting the stock solution to μM in ASTM. Live individuals were then exposed to Nile red working solution in the dark for 1 hr at 20°C. After incubation, animals were placed in 100 mL ASTM for 1 min to allow clearance of Nile red residuals. Following clearance, animals were placed individually in -mL centrifuge tubes, the remaining water was removed, and samples were sonicated in 300 μL of isopropanol. The homogenized extract was then centrifuged at 10,000 × g . We used 200 μL of supernatant to measure Nile red fluorescence using an excitation/emission wavelength of 530/590 nm and a microplate fluorescence reader (Synergy 2, BioTek). Each treatment had one animal per sample (10 replicates in total). For each quantification and treatment, 10 blanks (animals not exposed to Nile red) were used to account for background levels of fluorescence. After exposure to Nile red, images were taken in the area surrounding the midgut for visualization of lipid droplets. Fluorescence and bright file images were obtained using a Nikon SMZ1500 microscope and a Nikon Intensilight C-HGFI with a GFP filter (EX 472/30, EM 520/35; Nikon).

The ecdysteroid-binding pocket is located in the ligand binding domain of the EcR subunit , but EcR must be dimerised with a USP (or with an RXR) for high-affinity ligand binding to occur. In such circumstances, the binding of an agonist ligand triggers a conformational change in the C-terminal part of the EcR ligand-binding domain that leads to transcriptional activation of genes under ECRE control. [7] There is also a ligand-binding pocket in the corresponding domain of USP. Its natural ligand remains uncertain, and USPs appear to be locked permanently in an inactive conformation . [8]

50) During a stressful interval
A) TSH stimulates the adrenal cortex and medulla to secrete acetylcholine.
B) the alpha cells of islets secrete insulin and simultaneously the beta cells of the islets secrete glucagon.
C) ACTH stimulates the adrenal cortex, and neurons of the sympathetic nervous system stimulate the adrenal medulla.
D) the posterior pituitary gland secretes more growth hormones.
E) the calcium levels in the blood are increased due to actions of two antagonistic hormones, epinephrine and norepinephrine.

Ecdysteroid juvenile hormone

ecdysteroid juvenile hormone

50) During a stressful interval
A) TSH stimulates the adrenal cortex and medulla to secrete acetylcholine.
B) the alpha cells of islets secrete insulin and simultaneously the beta cells of the islets secrete glucagon.
C) ACTH stimulates the adrenal cortex, and neurons of the sympathetic nervous system stimulate the adrenal medulla.
D) the posterior pituitary gland secretes more growth hormones.
E) the calcium levels in the blood are increased due to actions of two antagonistic hormones, epinephrine and norepinephrine.

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