Robust Heat Shock Response in Chlamydia Lacking a Typical Heat Shock Sigma Factor

Cells reprogram their transcriptome in response to stress, such as heat shock. In free-living bacteria, the transcriptomic reprogramming is mediated by increased DNA-binding activity of heat shock sigma factors and activation of genes normally repressed by heat-induced transcription factors. In this study, we performed transcriptomic analyses to investigate heat shock response in the obligate intracellular bacterium Chlamydia trachomatis, whose genome encodes only three sigma factors and a single heat-induced transcription factor. Nearly one-third of C. trachomatis genes showed statistically significant (≥1.5-fold) expression changes 30 min after shifting from 37 to 45°C. Notably, chromosomal genes encoding chaperones, energy metabolism enzymes, type III secretion proteins, as well as most plasmid-encoded genes, were differentially upregulated. In contrast, genes with functions in protein synthesis were disproportionately downregulated. These findings suggest that facilitating protein folding, increasing energy production, manipulating host activities, upregulating plasmid-encoded gene expression, and decreasing general protein synthesis helps facilitate C. trachomatis survival under stress. In addition to relieving negative regulation by the heat-inducible transcriptional repressor HrcA, heat shock upregulated the chlamydial primary sigma factor σ66 and an alternative sigma factor σ28. Interestingly, we show for the first time that heat shock downregulates the other alternative sigma factor σ54 in a bacterium. Downregulation of σ54 was accompanied by increased expression of the σ54 RNA polymerase activator AtoC, thus suggesting a unique regulatory mechanism for reestablishing normal expression of select σ54 target genes. Taken together, our findings reveal that C. trachomatis utilizes multiple novel survival strategies to cope with environmental stress and even to replicate. Future strategies that can specifically target and disrupt Chlamydia’s heat shock response will likely be of therapeutic value.

Stressed out underground?: Transcriptomics illuminates the genome-wide response to heat stress in surface and subterranean diving beetles

Subterranean habitats are environmentally stable with respect to temperature, humidity, and the absence of light. The transition to a subterranean lifestyle might therefore be expected to cause considerable shifts in an organism's physiology; here, we investigate how subterranean colonisation affects thermal tolerance. Subterranean organisms might be at an increased risk of decline in the face of global temperature rises, but robust data on the fauna is lacking, particularly at the molecular level. In this study we compare the heat shock response of two species of diving beetle in the genus Paroster: one surface-dwelling (P. nigroadumbratus), the other restricted to a single aquifer (P. macrosturtensis). P. macrosturtensis has been previously established as having a lower thermal tolerance compared to surface-dwelling relatives, but the genomic basis of this difference is unknown. By sequencing transcriptomes of experimentally heat-shocked individuals and performing differential expression analysis, we demonstrate both species can mount a heat shock response at high temperatures (35C), in agreement with past survival experiments. However, the genes involved in these responses differ between species, and far greater genes are differentially expressed in the surface species, which may explain its more robust response to heat stress. In contrast, the subterranean species significantly upregulated the heat shock protein gene Hsp68 in the experimental setup under conditions it would likely encounter in nature (25C), suggesting it may be more sensitive to ambient stressors, e.g. handling. The results presented here contribute to an emerging narrative concerning weakened thermal tolerances in obligate subterranean organisms at the molecular level.

Enhancing the Shock Response Performance of Micromachined Silicon Resonant Accelerometers by Electrostatic Active Damping Control

This paper presents a micromachined silicon resonant accelerometer based on electrostatic active damping control, which can improve the shock response performance of the accelerometer. In the accelerometer, an electrostatic active damping structure and damping control circuit are designed to improve the equivalent damping coefficient of the system. System-level Simulink modeling and simulation of the accelerometer with an electrostatic active damping closed-loop control link were carried out. The simulation results indicate that the system can quickly return to normal output without an obvious vibration process after the shock. The fabricated and packaged accelerometer was connected to an external test circuit for shock performance testing. The stabilization time of the accelerometer after a 100 g, 3–5 ms half-sine shock was reduced from 19.8 to 5.6 s through use of the damping control. Furthermore, the change in deviation before and after the shock without damping control was 0.8197 mg, whereas it was 0.1715 mg with damping control. The experimental results demonstrate that the electrostatic active damping control can effectively improve the dynamic performance of the micromachined silicon resonant accelerometer.

Shock Reduction Technique on Thin Plate Structure by Wave Refraction Using an Elastic Patch

In general, bending waves transfer the largest portion of shock energy in a plate-like structure. This study proposes a new shock reduction method using an elastic patch designed to defocus the bending waves through the refraction of the waves so that it is possible to effectively reduce the propagating shock for a certain target area. Elastic patches of three different shapes were considered. The shock reduction performance of these patches was analytically, numerically, and experimentally investigated and compared. All results consistently showed that attached patches can effectively reduce passing waves for areas behind patches. Therefore, utilizing the proposed methods, we can reduce the transient shock response at certain target areas of various practical structures without degradation of structural stiffness or strength simply by bonding with an elastic patch.

Selenium Alleviated Oxidative Stress-Mediated Complex Poisoning Mechanism in Lead-Treated Chicken Kidneys: Inflammation, Heat Shock Response, and Autophagy

Lead (Pb) is a toxic environmental contaminant, and exerts renal toxicity. It is known that selenium (Se) performs antagonistic effect on Pb poisoning. However, biological events during the process were not well understood in chicken kidneys. The purpose of this research was to investigate mitigative mechanism of Se on Pb poisoning from point of view of oxidative stress, inflammation, heat shock response, and autophagy in chicken kidneys. One hundred and eighty male Hyline chickens (7-day-old) were randomly divided into the control group (offering standard diet and potable water), the Se group (offering Na2SeO3-added standard diet and potable water), the Pb group (offering standard diet and (CH3OO)2Pb-added potable water), and the Pb+Se group (offering Na2SeO3-added standard diet and (CH3OO)2Pb-added potable water). On 30th, 60th, and 90th days, kidneys were removed to perform the studies of histological structure, oxidative stress indicators, cytokines, heat shock proteins, and autophagy in the chicken kidneys. The experimental results indicated that Pb poisoning changed renal histological structure; decreased catalase, glutathione-s-transferase, and total antioxidative capacity activities; increased hydrogen peroxide content; induced mRNA and protein expression of heat shock proteins; inhibited interleukin (IL)-2 mRNA expression, and induced IL-4 and IL-12β mRNA expression; inhibited mammalian target of rapamycin mRNA and protein expression, and induced autophagy-related gene mRNA and protein expression in the chicken kidneys. Supplement of Se mitigated the above changes caused by Pb. In conclusion, Pb induced oxidative stress, inflammation, heat shock response, and autophagy and Se administration alleviated Pb poisoning through mitigating oxidative stress in the chicken kidneys.