Biology subjects

Christie, J.

Publications and source records attributed to Christie, J..

3 recordsLinked to original sources

bioRxiv2025

High protein diets early in life improve survival, reduce cannibalism, and increase growth and yield in farmed yellow mealworms

In the wild, animals may be able to compensate for nutritional inadequacies through foraging for novel resources; however, on farms, animals have more limited nutritional options. Therefore, providing adequate and accessible nutrition is essential to positive farmed animal welfare. Billions of yellow mealworms (Tenebrio molitor; Coleoptera: Tenebrionidae) are farmed as mini-livestock each year for use as food and feed. The major feedstock used, wheat bran, can sustain complete development of the species, but has been shown to have significantly lower protein content than yellow mealworms would typically self-select, particularly at early developmental stages. This can reduce growth, survival, and adult oviposition, and may contribute to high rates of cannibalistic behaviour among larvae (as larvae may have few options but to seek protein from the bodies of conspecifics). In this study, we use 20% nutritional yeast as a dietary protein supplement for larvae in early (0-4 weeks) and later life (4-8 weeks) to assess the effects on survival, growth rate, and rates of cannibalism, as well as any effects on growth, development timing, and adult body size. We also investigated the impact of this higher protein diet, when fed to either larvae or adults, on fecundity. We find that protein supplementation in larval diets increased survival by 23%, growth rate by 200%, and total biomass at eight weeks by up to 272%. Larval cannibalistic behaviour was reduced and development time was shorter. The high protein diet, whether fed to adults or to larvae, increased the number of offspring per female by 34-36%. Survival and growth benefits of protein supplementation were especially pronounced when fed to early juvenile instars, but can benefit mealworms across the entire first eight weeks of development. We highlight the need for further research into dietary protein supplementation for yellow mealworms across development to better align with their dietary choices, thereby improving fitness, yield, and welfare.

zoology↗

bioRxiv2021

Cytoplasmic Switch of ARS2 Isoforms Promotes Nonsense-Mediated mRNA Decay and Arsenic Sensitivity

The life of RNA polymerase II (RNAPII) transcripts is shaped by the dynamic formation of mutually exclusive ribonucleoprotein complexes (RNPs) that direct transcript biogenesis and turnover. A key regulator of RNA metabolism in the nucleus is the scaffold protein ARS2 (arsenic resistance protein 2), bound to the cap binding complex (CBC). We report here that alternative splicing of ARS2s intron 5, generates cytoplasmic isoforms that lack 270 amino acids from the N-terminal of the protein and are functionally distinct from nuclear ARS2. Switching of ARS2 isoforms within the CBC in the cytoplasm has dramatic functional consequences, changing ARS2 from a NMD inhibitor to a NMD promoter that enhances the binding of UPF1 to NCBP1, ERF1 and DHX34, favouring SURF complex formation, SMG7 recruitment and transcript degradation. ARS2 isoform exchange is also relevant during arsenic stress, where cytoplasmic ARS2 promotes a global response to arsenic in a CBC-independent manner. We propose that ARS2 isoform switching promotes the proper recruitment of RNP complexes during NMD and the cellular response to arsenic stress. The existence of non-redundant ARS2 isoforms is relevant for cell homeostasis, stress response, and cancer treatment.

molecular biology↗

bioRxiv2017

Mitigating Mitochondrial Genome Erosion Without Recombination

Mitochondria are ATP-producing organelles of bacterial ancestry that played a key role in the origin and early evolution of complex eukaryotic cells. Most modern eukaryotes transmit mitochondrial genes uniparentally, often without recombination among genetically divergent organelles. While this asymmetric inheritance maintains the efficacy of purifying selection at the level of the cell, the absence of recombination could also make the genome susceptible to Mullers ratchet. How mitochondria escape this irreversible defect accumulation is a fundamental unsolved question. Occasional paternal leakage could in principle promote recombination, but it would also compromise the purifying-selection benefits of uniparental inheritance. We assess this tradeoff using a stochastic population-genetic model. In the absence of recombination, uniparental inheritance of freely segregating genomes mitigates mutational erosion, while paternal leakage exacerbates the ratchet effect. Mitochondrial fusion-fission cycles ensure independent genome segregation, improving purifying selection. Paternal leakage provides opportunity for recombination to slow down the mutation accumulation, but always at a cost of increased steady-state mutation load. Our findings indicate that random segregation of mitochondrial genomes under uniparental inheritance can effectively combat the mutational meltdown, and that homologous recombination under paternal leakage might not be needed.

genetics↗