Structural and functional conservation of key domains in InsP3 and ryanodine receptors

Spodopteraexigua, a multifeeding insect pest, has developed a high level of resistance to chlorantraniliprole, which is a benzoylurea insecticide that targets the ryanodine receptors (RyRs). Herein, the resistant strain (SE-Sel) and sensitive strain (SE-Sus) were obtained by bidirectional screening for six generations. The potential oviposited eggs and oviposition rate of the SE-Sel strain were dramatically lower than those of the SE-Sus strain; on the contrary, the weights of prepupae and preadult were significantly increased. As a post-mating response, the higher number of non-oviposited eggs in the SE-Sel strain was caused by a lower mating rate. In addition, the expression levels of vitellogenin (SeVg) and its receptor (SeVgR) in the SE-Sel strain were consistently lower than those in the SE-Sus strain. An RyRI4743M mutation, contributing to the resistance to chlorantraniliprole, was located in the S3 transmembrane segments and might have affected the release of calcium ions; it led to the upregulated expression of the neuropeptide SeNPF and its receptor SeNPFR, and the mating and oviposition rate were significantly recovered when the SeNPF was knocked down though RNA interference (RNAi) in the male adult of the SE-Sel strain. Moreover, the expression of the juvenile hormone-binding proteins SeJHBWDS3 and SeJHBAN in the male adult of the SE-Sel strain was significantly decreased, which proved the existence of a fitness cost from another angle. Therefore, these results indicate that the fitness cost accompanied by chlorantraniliprole resistance in S. exigua may be related to the decrease in mating desire due to SeNPF overexpression.

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Different intracellular localization of inositol 1,4,5-trisphosphate and ryanodine receptors in cardiomyocytes.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(18)53722-4 ◽

1993 ◽

Vol 268 (5) ◽

pp. 3499-3506

Author(s):

Y. Kijima ◽

A. Saito ◽

T.L. Jetton ◽

M.A. Magnuson ◽

S. Fleischer

Keyword(s):

Intracellular Localization ◽

Ryanodine Receptors ◽

Inositol 1,4,5 Trisphosphate

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Extended junctional sarcoplasmic reticulum of avian cardiac muscle contains functional ryanodine receptors.

Journal of Biological Chemistry ◽

10.1016/s0021-9258(17)42073-4 ◽

1994 ◽

Vol 269 (3) ◽

pp. 1627-1634

Author(s):

J. Junker ◽

J.R. Sommer ◽

M. Sar ◽

G. Meissner

Keyword(s):

Sarcoplasmic Reticulum ◽

Cardiac Muscle ◽

Ryanodine Receptors ◽

Junctional Sarcoplasmic Reticulum

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Deregulation of Ca2+-Signaling Systems in White Adipocytes, Manifested as the Loss of Rhythmic Activity, Underlies the Development of Multiple Hormonal Resistance at Obesity and Type 2 Diabetes

International Journal of Molecular Sciences ◽

10.3390/ijms22105109 ◽

2021 ◽

Vol 22 (10) ◽

pp. 5109

Author(s):

Egor A. Turovsky ◽

Maria V. Turovskaya ◽

Vladimir V. Dynnik

Keyword(s):

Cell Size ◽

Ryanodine Receptors ◽

Fluorescent Microscopy ◽

Rhythmic Activity ◽

Ip3 Receptors ◽

Signaling Systems ◽

White Adipocytes ◽

Inhibitory Analysis ◽

Hormonal Resistance ◽

The Impact

Various types of cells demonstrate ubiquitous rhythmicity registered as simple and complex Ca2+-oscillations, spikes, waves, and triggering phenomena mediated by G-protein and tyrosine kinase coupled receptors. Phospholipase C/IP3-receptors (PLC/IP3R) and endothelial NO-synthase/Ryanodine receptors (NOS/RyR)–dependent Ca2+ signaling systems, organized as multivariate positive feedback generators (PLC-G and NOS-G), underlie this rhythmicity. Loss of rhythmicity at obesity may indicate deregulation of these signaling systems. To issue the impact of cell size, receptors’ interplay, and obesity on the regulation of PLC-G and NOS-G, we applied fluorescent microscopy, immunochemical staining, and inhibitory analysis using cultured adipocytes of epididumal white adipose tissue of mice. Acetylcholine, norepinephrine, atrial natriuretic peptide, bradykinin, cholecystokinin, angiotensin II, and insulin evoked complex [Ca2+]i responses in adipocytes, implicating NOS-G or PLC-G. At low sub-threshold concentrations, acetylcholine and norepinephrine or acetylcholine and peptide hormones (in paired combinations) recruited NOS-G, based on G proteins subunits interplay and signaling amplification. Rhythmicity was cell size- dependent and disappeared in hypertrophied cells filled with lipids. Contrary to control cells, adipocytes of obese hyperglycemic and hypertensive mice, growing on glucose, did not accumulate lipids and demonstrated hormonal resistance being non responsive to any hormone applied. Preincubation of preadipocytes with palmitoyl-L-carnitine (100 nM) provided accumulation of lipids, increased expression and clustering of IP3R and RyR proteins, and partially restored hormonal sensitivity and rhythmicity (5–15% vs. 30–80% in control cells), while adipocytes of diabetic mice were not responsive at all. Here, we presented a detailed kinetic model of NOS-G and discussed its control. Collectively, we may suggest that universal mechanisms underlie loss of rhythmicity, Ca2+-signaling systems deregulation, and development of general hormonal resistance to obesity.

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