scholarly journals A positive feedback loop between Dumbfounded and Rolling pebbles leads to myotube enlargement in Drosophila

2005 ◽  
Vol 169 (6) ◽  
pp. 909-920 ◽  
Author(s):  
Sree Devi Menon ◽  
Zalina Osman ◽  
Kho Chenchill ◽  
William Chia
Keyword(s):  
Positive Feedback ◽  
Feedback Loop ◽  
Transmembrane Protein ◽  
Coiled Coil ◽  
Tetratricopeptide Repeat ◽  
Positive Feedback Loop ◽  
Coiled Coil Domain ◽  
Fusion Site ◽  
Fusion Competent Myoblasts

In Drosophila, myoblasts are subdivided into founders and fusion-competent myoblasts (fcm) with myotubes forming through fusion of one founder and several fcm. Duf and rolling pebbles 7 (Rols7; also known as antisocial) are expressed in founders, whereas sticks and stones (SNS) is present in fcm. Duf attracts fcm toward founders and also causes translocation of Rols7 from the cytoplasm to the fusion site. We show that Duf is a type 1 transmembrane protein that induces Rols7 translocation specifically when present intact and engaged in homophilic or Duf–SNS adhesion. Although its membrane-anchored extracellular domain functions as an attractant and is sufficient for the initial round of fusion, subsequent fusions require replenishment of Duf through cotranslocation with Rols7 tetratricopeptide repeat/coiled-coil domain-containing vesicles to the founder/myotube surface, causing both Duf and Rols7 to be at fusion sites between founders/myotubes and fcm. This implicates the Duf–Rols7 positive feedback loop to the occurrence of fusion at specific sites along the membrane and provides a mechanism by which the rate of fusion is controlled.

scholarly journals Heat hypersensitivity of ryanodine receptor type 1 mutants implicated in malignant hyperthermia

2020 ◽  
Author(s):  
Kotaro Oyama ◽  
Vadim Zeeb ◽  
Toshiko Yamazawa ◽  
Takashi Murayama ◽  
Hideto Oyamada ◽  
...  
Keyword(s):  
Malignant Hyperthermia ◽  
Ryanodine Receptor ◽  
Positive Feedback ◽  
Intracellular Signaling ◽  
Feedback Loop ◽  
Local Heat ◽  
Receptor Type ◽  
Positive Feedback Loop ◽  
Hek 293

AbstractCellular heat-sensing is a universal strategy for avoiding thermal damage and adapting to environments by regulating thermogenic activities. If heat-sensing results in the acceleration of processes governing cellular thermogenesis, hyperthermia can occur. However, how this positive feedback loop contributes to hyperthermia development, especially the gap between heat-sensing and thermogenesis, remains largely unknown. Here, we show that an optically controlled local heat pulse induces an intracellular Ca2+ burst in cultured HEK 293 cells overexpressing ryanodine-receptor-type-1 (RyR1) mutants related to the life-threatening illness malignant hyperthermia (MH), and that the Ca2+ burst originates from heat-induced Ca2+-release (HICR) because of the mutant channels’ heat hypersensitivity. Furthermore, the heat hypersensitivity of the four RyR1 mutants was ranked, highlighting the complexity of MH. Our findings reveal the novel cellular heat-sensing mechanism, HICR, is essential for the functional positive feedback loop causing MH, suggesting a well-tuned HICR is fundamental for heat-mediated intracellular signaling.

scholarly journals Arabidopsis vascular complexity and connectivity controls PIN-FORMED1 dynamics and lateral vein patterning during embryogenesis

Development ◽  
2021 ◽  
Author(s):  
Makoto Yanagisawa ◽  
Arthur Poitout ◽  
Marisa S. Otegui
Keyword(s):  
Plasma Membrane ◽  
Positive Feedback ◽  
Feedback Loop ◽  
Transmembrane Protein ◽  
Vascular Development ◽  
Lateral Vein ◽  
Dependent Manner ◽  
Positive Feedback Loop ◽  
Vein Patterning ◽  
Auxin Efflux Carrier

Arabidopsis VASCULATURE COMPLEXITY AND CONNECTIVITY (VCC) is a plant-specific transmembrane protein that controls the development of veins in cotyledons. Here we show that the expression and localization of the auxin efflux carrier PIN-FORMED1 (PIN1) is altered in vcc developing cotyledons and that overexpression of PIN1-GFP partially rescues vascular defects of vcc in a dosage-dependent manner. Genetic analyses suggest that VCC and PINOID (PID), a kinase that regulates PIN1 polarity, are both required for PIN1-mediated control of vasculature development. VCC expression is upregulated by auxin, likely as part of a positive feedback loop for the progression of vascular development. VCC and PIN1 localized to the plasma membrane in pre-procambial cells but are actively redirected to vacuoles in procambial cells for degradation. In the vcc mutant, PIN1 failed to properly polarize in pre-procambial cells during the formation of basal strands and instead, it is prematurely degraded in vacuoles. VCC plays a role in localization and stability of PIN1, which is critical for the transition of pre-procambial into procambial cells involved in the formation of basal lateral strands in embryonic cotyledons.

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