Temperature-sensitive Pathway Research Articles

Temperature-sensitive pathways may be involved in duck embryonic developmental recovery from blastoderm dormancy during hatching

ABSTRACT 1. Birds’ newly oviposited blastoderms can survive several weeks in a dormant state during low-temperature storage. Previous studies demonstrated that there is a critical temperature range from 19 to 27°C for chicken embryos. Within this range, the embryo will diapause in a dormant state; once the temperature rises above this range, the blastoderm will break dormancy. 2. Clarifying the mechanism that initiates duck embryo developmental recovery from blastoderm dormancy will be helpful to change temperature control to improve hatching in poultry production. It was hypothesised that there might be some temperature-sensitive genes involved in initiating duck embryo developmental recovery from blastoderm dormancy. 3. To test this hypothesis, the transcriptome of the newly oviposited duck blastoderm and duck embryo (incubated for 48 hours) were sequenced to screen for differentially expressed genes with functions that had been predicted by bioinformatics. 4. The results showed that there were 2416 differentially expressed genes between the two groups, 53 of which were involved in temperature-sensitive pathways. The protein-protein interaction network combined these 53 temperature-sensitive genes and another group of 65 genes, which enriched the development pathway. These results suggested that temperature-sensitive genes may be involved in growth and development related pathways.

Abstract 283: Novel Mechanism of Low-Density Lipoprotein--Derived Cholesteryl Ester Uptake and Hydrolysis During Macrophage Foam Cell Formation

Macrophage foam cells are a defining pathologic feature of atherosclerotic lesions. Classically, scavenger receptor-mediated uptake of oxidized or enzyme-modified LDL is cited as a mechanism for foam cell formation. Recent studies have demonstrated that at high concentrations, native LDL can also induce macrophage lipid accumulation. LDL particles are taken up by macrophages as part of bulk fluid pinocytosis. However, the uptake and metabolism of cholesterol derived from native LDL during macrophage foam cell formation has not been clearly defined. Previous studies suggested that selective CE uptake might contribute to cholesterol uptake independently of LDL endocytosis. In this study we demonstrate that the majority of cholesterol taken up from LDL is acquired by selective CE uptake and not by pinocytosis and LDL degradation. CE uptake does not saturate at high LDL concentrations and is not down-regulated during cholesterol accumulation. LDL modification and scavenger receptors do not appear to play a major role in macrophage selective CE uptake. Following uptake from LDL, CE is rapidly hydrolyzed in macrophages by a novel chloroquine- and temperature-sensitive pathway. Our findings suggest that selective CE uptake plays a major role in macrophage cholesterol homeostasis during foam cell formation.

The Neurospora crassa Circadian Clock

The filamentous fungus Neurospora crassa is one of a handful of model organisms that has proven tractable for dissecting the molecular basis of a eukaryotic circadian clock. Work on Neurospora and other eukaryotic and prokaryotic organisms has revealed that a limited set of clock genes and clock proteins are required for generating robust circadian rhythmicity. This molecular clockwork is tuned to the daily rhythms in the environment via light- and temperature-sensitive pathways that adjust its periodicity and phase. The circadian clockwork in turn transduces temporal information to a large number of clock-controlled genes that ultimately control circadian rhythms in physiology and behavior. In summarizing our current understanding of the molecular basis of the Neurospora circadian system, this chapter aims to elucidate the basic building blocks of model eukaryotic clocks as we understand them today.

Metabolic stability and antigenic modulation of nicotinic acetylcholine receptors on bovine adrenal chromaffin cells.

Bovine adrenal chromaffin cells have nicotinic acetylcholine receptors (AChRs) that are activated by the splanchnic nerve, resulting in release of catecholamines from the cells. Examination of the AChRs can provide information about the regulation and turnover of synaptic components on neurons and endocrine cells. Previous studies have shown that mAb 35 recognizes the AChR on the cells. Here we show that mAb 35 can remove AChRs from the surface of the cells by antigenic modulation, and that the modulation can be used together with other methods to examine the stability and turnover of the receptors in the plasma membrane. Unexpectedly, the results indicate a disparity between the rate at which AChRs reappear on the cells and the rate at which the ACh response recovers after preexisting AChRs have been removed. Exposure of bovine adrenal chromaffin cultures to mAb 35 results in a parallel decrease in the magnitude of the nicotinic response and the number of AChRs on the cells. The decrease depends on the concentration and divalence of mAb 35, and on the time and temperature of the incubation. The antibody induces receptor aggregation in the plasma membrane under conditions where receptor loss subsequently occurs. After binding to receptor, mAb 35 appears to be internalized, degraded, and released from the cells through a temperature sensitive pathway that requires lysosomal function. These features are characteristic of antigenic modulation. Appearance of new AChRs on the cells either after antigenic modulation or after blockade of existing AChRs with monovalent antibody fragments occurs at a rate equivalent to 3% of the receptors present on control cells per hour. The rate of receptor loss from the cells was measured in the presence of either tunicamycin or puromycin to block appearance of new receptors. Both conditions indicated a receptor half-life of approximately 24 h and a rate of loss of approximately 3%/h. The finding that the rate of receptor loss equaled the rate of receptor appearance was consistent with the observation that the total number of AChRs on untreated cells did not increase with time. In the presence of tunicamycin, loss of receptor-mediated response to nicotine also occurred with a half-time of 24 h. Paradoxically, the rate of recovery of the nicotinic response, determined using two procedures, was more than twice as great as the rate at which new AChRs appeared on the cells.(ABSTRACT TRUNCATED AT 400 WORDS)