Societal Impact StatementSandalwood and other high value tree species are under significant threat from illegal harvest. Illegal logging is an increasing problem contributing to deforestation, biodiversity loss, human rights abuses and funding transnational crime. Successful prosecution of illegal logging is hindered by a lack of methods to provide evidence of the origin of timber. New analytical techniques have been developed to trace timber back to its source. These methods, together with the establishment of sustainable sources of forest resources, can help protect vulnerable species by providing evidence to prosecute illegal harvest and ensure that commercially available forest products come from sustainable sources.SummarySandalwood is highly valued for its fragrant oil and has a long history of cultural and economic importance in many regions of the world. Historical overharvest and poor management have depleted natural populations of sandalwood, which are slow to regenerate. The increasing establishment of plantation sandalwood creates an alternative resource for the sandalwood industry while potentially relieving harvesting pressure on natural stands. Due to the high demand for sandalwood, remaining wild populations are still under threat from illegal logging and methods to identify the source of harvested sandalwood are needed. Laws and regulations aimed at preventing illegal harvest and possession of sandalwood have been put in place but cannot be enforced without the forensic tools to independently verify claimed origin or product quality. The high value of sandalwood combined with the difficulties in enforcing illegal logging laws makes these species particularly vulnerable to poaching. There is an immediate need to develop tools that can identify illegally sourced and adulterated sandalwood products. This paper reviews the current and developing scientific tools that can help identify and control illegal activity in sandalwood supply chains and provides recommendations for future research. Topics include isotope and DNA analysis for tracing illegally harvested sandalwood, chemical profiling for quality control of sandalwood oils, network and policy development to establish a framework for future regulation of the sandalwood trade.

This study aimed to clarify the mechanisms contributing to ontogenetic differences in red locomotor muscle metabolic heat production in regionally endothermic tunas. To address this, the scaling of citrate synthase (CS), cytochrome c oxidase (COX) and pyruvate kinase (PK), enzymes involved in cellular respiration, in the red and white locomotor muscle of young (~ 2 to ~ 16 months of age) Pacific bluefin tuna (Thunnus orientalis) during the ontogeny of red muscle endothermy was investigated. On a mass-specific basis (units g−1 muscle tissue), CS activity scaled negatively with body mass with scaling coefficients of −0.12 for red muscle and −0.21 for white muscle, whereas COX activity did not scale in either muscle type and PK activity scaled positively in white muscle, with a scaling coefficient of 0.09, but did not scale in red muscle. Thus, proxies for mass-specific metabolic heat production potential from cellular respiration either decreased or remained constant in the red muscle during the ontogeny of red muscle endothermy. In contrast, total red muscle mass and total CS and COX activities all scaled positively with body mass, with scaling coefficients of 0.90, 0.78 and 0.92, respectively, and each of these correlated positively with the magnitude of the red muscle thermal excess. Thus, increasing total, but not mass-specific, metabolic heat production capacity contributed to the increasing red muscle thermal excess with increasing body size in juvenile T. orientalis. Additionally, transcript abundance was a poor predictor of enzyme activity. Thus, transcriptional regulation played a limited role in determining the enzymes’ scaling relationships.

Tunas can elevate their red (slow-twitch, oxidative) skeletal muscle, visceral and cranial temperatures significantly above the ambient water temperature (Ta) with the aid of specialized blood vessels (retia mirabilia) that conserve metabolic heat. The ontogeny of this phenomenon, known as regional endothermy, was studied in young [18.5–62.5 cm fork length (FL), 71–5350 g body mass, 2–16 months of age] Pacific bluefin tuna (Thunnus orientalis). Maximal red muscle, visceral and cranial temperatures were measured in parallel with measuring red muscle mass and the size of the red muscle and visceral retia. The maximal thermal excess (maximal tissue temperature – Ta) increased from 1.1 ± 0.3 °C (mean ± SD) to 11.1 ± 3.4 °C in the red muscle, from 0.6 ± 0.3 °C to 3.5 ± 1.4 °C in the viscera and from 0.5 ± 0.4 °C to 2.0 ± 0.6 °C in the cranium in the smallest individuals compared with the largest. Thus, red muscle endothermy was well developed, but visceral and cranial endothermy were still developing, in the largest individuals studied. The scaling coefficients, relative to body mass, for total red muscle mass (0.90 ± 0.03, mean ± SE), red muscle rete (RMR) length (0.84 ± 0.06), maximum number of RMR blood vessel rows (0.43 ± 0.04) and visceral rete cross-sectional area (0.90 ± 0.08), indicated negative allometry for total red muscle mass (< 1.0) but positive allometry for the length of the red muscle retia (> 0.33) and the area of the visceral rete (> 0.67).

Peroxiredoxins are antioxidant enzymes that use redox active Cys residues to reduce H2O2 and various organic hydroperoxides to less reactive products, and thereby protect cells against oxidative stress. In yeasts and mammals, the Prx1 proteins are sensitive to hyperoxidation and consequent loss of their peroxidase activity whereas in most bacteria they are not. In this paper we report the characterization of the Prx1 family in the non-parasitic protist Tetrahymena thermophila. In this organism, four genes potentially encoding Prx1 have been identified. In particular, we show that the mitochondrial Prx1 protein (Prx1m) from T. thermophila is relatively robust to hyperoxidation. This is surprising given that T. thermophila is a eukaryote like yeasts and mammals. In addition, the proliferation of the T. thermophila cells was relatively robust to inhibition by H2O2, cumene hydroperoxide and plant natural products that are known to promote the production of H2O2. In the presence of these agents, the abundance of the T. thermophila Prx1m protein was shown to increase. This suggested that the Prx1m protein may be protecting the cells against oxidative stress. There was no evidence for any increase in Prx1m gene expression in the stressed cells. Thus, increasing protein stability rather than increasing gene expression may explain the increasing Prx1m protein abundance we observed.