Biology subjects

Hird, C.

Publications and source records attributed to Hird, C..

5 recordsLinked to original sources

bioRxiv2024

Microalgal biofilm induces larval settlement in the model marine worm Platynereis dumerilii

A free-swimming larval stage features in many marine invertebrate life cycles. To transition to a seafloor-dwelling juvenile stage, larvae need to settle out of the plankton, guided by specific environmental cues that lead them to an ideal habitat for their future life on the seafloor. Although the marine annelid Platynereis dumerilii has been cultured in research labs since the 1950s and has a free-swimming larval stage, specific environmental cues that induce settlement in this nereid worm are yet to be identified. Here we demonstrate that microalgal biofilm is a key settlement cue for P. dumerilii larvae, inducing earlier onset of settlement, and enhancing subsequent juvenile growth as a primary food source. We tested the settlement response of P. dumerilii to 40 different strains of microalgae, predominantly diatom species, finding that P. dumerilii have species-specific preferences in their choice of settlement substrate. The most effective diatom species for inducing P. dumerilii larval settlement were benthic pennate species including Grammatophora marina, Achnanthes brevipes, and Nitzschia ovalis. The identification of specific environmental cues for P. dumerilii settlement enables a link between its ecology and the sensory and nervous system signalling that regulate larval behaviour and development. Incorporation of diatoms into P. dumerilii culture practices will improve the husbandry of this marine invertebrate model.

zoology↗

bioRxiv2023

Cold-induced skin darkening does not protect amphibian larvae from UV-associated DNA damage

O_LIMany amphibian declines are correlated with increasing levels of ultraviolet radiation (UVR). While disease is often implicated in declines, environmental factors such as temperature and UVR play an important role in disease epidemiology. C_LIO_LIThe mutagenic effects of UVR exposure on amphibians are worse at low temperatures. Amphibians from cold environments may be more susceptible to increasing UVR. However, larvae of some species demonstrate cold acclimation, reducing UV-induced DNA damage at low temperatures. Understanding of the mechanisms underpinning this response is lacking. C_LIO_LIWe reared Limnodynastes peronii larvae in cool (15{degrees}C) or warm (25{degrees}C) waters before acutely exposing them to 1.5 h of high intensity (80 W cm-2) UVBR. We measured the colour of larvae and mRNA levels of a DNA repair enzyme. We reared larvae at 25{degrees}C in black or white containers to elicit a skin colour response, and then measured DNA damage levels in the skin and remaining carcass following UVBR exposure. C_LIO_LICold acclimated larvae were darker and displayed lower levels of DNA damage than warm-acclimated larvae. There was no difference in CPD-photolyase mRNA levels between cold- and warm-acclimated larvae. Skin darkening in larvae did not reduce larval accumulation of DNA damage following UVR exposure. C_LIO_LIOur results showed that skin darkening alone does not explain cold-induced reductions in UV-associated DNA damage in L. peronii larvae. Beneficial cold-acclimation is more likely underpinned by increased CPD-photolyase abundance and/or increased photolyase activity at low temperatures. C_LI Research HighlightsO_LIL. peroniii larvae darken when exposed to cold temperatures C_LIO_LIDarker larvae were not protected from the effects of UV on DNA damage C_LIO_LICold acclimation of larvae when exposed to UV is likely driven by DNA repair enzymes not melanin C_LI

molecular biology↗

bioRxiv2023

Thermal compensation reduces DNA damage in UV-exposed amphibian larvae: implications for high latitudinal and altitudinal species

1. Increases in ultraviolet radiation (UVR) correlate spatially and temporally with global amphibian population declines and interact with other stressors such as disease and temperature. Declines have largely occurred in high-altitude areas associated with greater UVR and cooler temperatures. 2. UVR is a powerful mutagenic harming organisms largely by damaging DNA. When acutely exposed to UVR at cool temperatures, amphibian larvae have increased levels of DNA damage. Amphibians may be able to compensate for the depressive effects of temperature on DNA damage through thermal acclimatisation, but it is unknown whether they or other ectotherms have this capacity. 3. We reared striped marsh frog larvae (Limnodynastes peronii) in warm (25{degrees}C) and cool (15{degrees}C) temperatures under either a low or moderate daily dose of UVR (10 and 40 {micro}W cm-2 UV-B for 1 h at midday, respectively) for 18-20 days and then measured immediate DNA damage resulting from an acute high UVR dose (80 {micro}W cm-2 UV-B for 1.5 h) at a range of test temperatures (10, 15, 20, 25, and 30{degrees}C). 4. Larvae acclimated to 15{degrees}C and exposed to UVR at 15{degrees}C completely compensated UVR-induced DNA damage compared with 25{degrees}C acclimated larvae exposed to UVR at 25{degrees}C. Additionally, warm-acclimated larvae had higher CPDs than cold-acclimated larvae across test temperatures, which indicated a cost of living in warmer temperatures. In contrast, larvae reared under chronic elevated UVR levels showed no evidence of UVR acclimation resulting in lower DNA damage following an acute high UVR exposure. 5. Our finding that thermal acclimation in L. peronii larvae compensated UVR-induced DNA damage at low temperatures suggested that aquatic ectotherms living in cool temperatures may be more resilient to high UVR than previously realised. 6. We suggested individuals or species with less capacity for thermal acclimation of DNA repair mechanisms may be more at risk if exposed to changing thermal and UVR exposure regimes but cautioned that thermal acclimation of DNA repair mechanisms may not always be beneficial.

zoology↗

bioRxiv2022

Temperature causes species-specific responses to UV-induced DNA damage in amphibian larvae

Anthropogenic ozone depletion has led to a 2-5% increase in ultraviolet B radiation (UVBR) levels reaching the earths surface. Exposure to UVBR causes harmful DNA damage in amphibians, but this is minimized by DNA repair enzymes such as thermally sensitive CPD-photolyase, with cool temperatures slowing repair rates. It is unknown whether amphibian species differ in the repair response to a given dose of UVBR across temperatures. We reared larvae of three species (Limnodynastes peronii, Limnodynastes tasmaniensis, and Platyplectrum ornatum) at 25{degrees}C and acutely exposed them to 80 W cm-2 UVBR for 2 h at either 20{degrees}C or 30{degrees}C. UVBR-mediated DNA damage was measured as larvae repaired damage in photoreactive light at their exposure temperatures. Cool temperatures increased DNA damage in all two species and slowed DNA repair rate in P. ornatum. The magnitude of DNA damage incurred from UVBR was species-specific. P. ornatum had the lowest CPDs and DNA repair rates, and the depressive effects of low temperature on photorepair were greater in L. tasmaniensis. Considering the susceptibility of most aquatic organisms to UVBR, this research highlighted a need to consider the complexity of species-specific physiology when forecasting the influence of changing UVBR and temperature in aquatic ecosystems.

molecular biology↗

bioRxiv2022

The role of environmental calcium in the extreme acid tolerance of northern banjo frog (Limnodynastes terraereginae) larvae

Many aquatically respiring animals inhabiting low pH waters can suffer acute inhibition of ion uptake and loss of branchial (gill) epithelial integrity, culminating in a fatal, rapid loss of body Na+. Environmental calcium levels ([Ca2+]e) are pivotal in maintaining branchial junction integrity, with supplemental Ca2+ reversing the negative effects of low pH in some animals. Tolerance of some naturally acidic environments by aquatic animals is further complicated by low [Ca2+]e, yet many of these environments are surprisingly biodiverse. How these animals overcome the combined damaging actions of low pH and low environmental Ca2+ remains unknown. Here, we examined the effects of [Ca2+]e on the response to low pH in larvae of the highly acid tolerant frog Limnodynastes terraereginae. Acute exposure to low pH water in the presence of low [Ca2+]e increased net Na+ efflux. Provision of additional [Ca2+]e reduced net Na+ efflux, but the effect was saturable. Acclimation to both low and high [Ca2+]e improved the resistance of larvae to Na+ efflux at low pH. Inhibition of apical Ca2+ uptake by ruthenium red resulted in an abrupt loss of tolerance to low pH in larvae acclimated to low pH water. Acclimation to acidic water increased branchial gene expression of the intracellular Ca2+ transport protein calbindin, consistent with a role for increased transcellular Ca2+ trafficking in the tolerance of acidic water. This study confirmed the physiological challenge of low [Ca2+]e on branchial integrity in acidic waters and highlighted a potential role for maintenance of transcellular Ca2+ uptake in the acid tolerance of L. terraereginae. Summary statementTolerance of naturally acidic, dilute, and soft waters by larvae of the frog Limnodynastes terraereginae involves adaptations to the branchial calcium transport pathway which protects intercellular junctions against damage.

physiology↗