Physiological responses to fluctuating temperatures are characterized by distinct transcriptional profiles in a solitary bee

Abstract

Exposure to stressful low temperatures during development can result in the accumulation of deleterious physiological effects called chill injury. Metabolic imbalances, disruptions in ion homeostasis and oxidative stress contribute to the increased mortality of chill-injured insects. Interestingly, survival can be significantly increased when chill-susceptible insects are exposed to a daily warm-temperature pulse during chilling. We hypothesize that warm pulses allow for the repair of damage associated with chill injury. Here, we describe transcriptional responses during exposure to a fluctuating thermal regime, relative to constant chilled temperatures, during pupal development in the alfalfa leafcutting bee, , using a combination of RNA-seq and qPCR. Pupae were exposed to either a constant, chilled temperature of 6°C, or 6°C with a daily pulse of 20°C for 7 days. RNA-seq after experimental treatment revealed differential expression of transcripts involved in construction of cell membranes, oxidation-reduction and various metabolic processes. These mechanisms provide support for shared physiological responses to chill injury across taxa. The large number of differentially expressed transcripts observed after 7 days of treatment suggests that the initial divergence in expression profiles between the two treatments occurred upstream of the time point sampled. Additionally, the differential expression profiles observed in this study show little overlap with those differentially expressed during temperature stress in the diapause state of While the mechanisms governing the physiological response to low-temperature stress are shared, the specific transcripts associated with the response differ between life stages.

Mechanisms underpinning the beneficial effects of fluctuating thermal regimes in insect cold tolerance

“…myofilin isoform b, sestrin-like and DNA damage-binding protein 1) suggests that individuals may experience DNA damage, potentially caused by increased levels of reactive oxygen species (ROS). This was not observed in FTR-exposed insects (Torson et al, 2017). Whether FTR allows cold-induced genotoxicity to be repaired needs confirmation.…”

“…aquaporins and transmembrane proteins), as well as increased expression of desaturases (i.e. enzymes capable of catalyzing the desaturation of fatty acids), indicating that the CLTand FTR-exposed bees may have distinct membrane structure and functionality (Torson et al, 2017). Together, these data suggest that one of the mechanisms of FTR is to repair putative cold-induced membrane alterations or to change membrane structure to optimise and maintain functions at low temperature.…”

“…Transcripts coding for structural constituents of the cytoskeleton were also expressed during FTR (e.g. actin, dynein, myosin, myofilin) (Torson et al, 2015(Torson et al, , 2017.…”

Effect of nest microclimate temperatures on metabolic rates of small carpenter bees, Ceratina calcarata (Hymenoptera: Apidae)

“…A negative correlation between metabolic and developmental rates in Ceratina exposed to high developmental temperatures suggests decoupling of metabolic and developmental rates. The significantly higher metabolic rates of sunny-nest bees in high temperatures may indicate that the bees adapt to the high temperatures they sometimes experience, perhaps by activating biochemical pathways to produce thermal protectants, such as heat-shock proteins (Hofmann and Todgham 2010;Torson et al 2017). Such Table 2, model D. Bees from different field treatments had similar metabolic rates, but at high test temperatures (40°C), bees raised in sun had significantly higher metabolic rates than those raised in shade.…”

Thermal stress causes DNA damage and mortality in a tropical insect

“…Upregulation of several transcripts in cold-stressed bees (e.g. myofilin isoform b, sestrin-like and DNA damage-binding proteins) suggests that insects may experience DNA damage, potentially caused by increased levels of reactive oxygen species (ROS) (Torson et al, 2017). Whether cold and freezing stress can damage DNA has not yet been examined, other than at chromosomal level.…”