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Heavy metal pollution has become increasingly prominent, and bioremediation of heavy metal polluted areas is urgently needed. Broussonetia papyrifera is a pioneer tree species for vegetation restoration in the tailings area, while its molecular mechanism of heavy metal adaptation is not clear. Here, we report that a R2R3 MYB from B. papyrifera (BpMYB1) is involved in Cd accumulation by controlling the down-stream genes and mineral accumulation. Overexpression of BpMYB1 in B. papyrifera resulted in a significant increase in Cd accumulation and multiple gene transcription. Among the up-regulated genes, BpMYB1 could bind to ferrochelatase (BpFC2), basic helix-loop-helix transcription factor bHLH93 (BpbHLH93), and basic leucine zipper transcription factor bZIPs (BpbZIP1 , BpbZIP-CPC1) by recognizing TATCCAOSAMY (TATCCA) motif and related promoter segments. Further investigations revealed that overexpression of BpbZIP1 promotes the absorption of Cd, BpMYB1 regulate Cd uptake in plant relating to Fe accumulation without Fe-deficiency pathway via recognizing the downstream BpbHLH93 and involving in PCs biosynthetic pathway via recognizing the target BpFC2. Moreover, the Cd response effect mediated by BpMYB1 was boosted by interacting with a DELLA protein BpGAI1, a vital member of GA signaling. These results provide new insights into the molecular feedback mechanisms underlying BpMYB1-BpGAI1 controlled Cd uptake in plants, which will benefit for phytoremediation of Cd polluted soil. [Display omitted] • BpMYB1 overexpression benefits for Cd enrichment and tolerance of B. papyrifera. • BpMYB1 could regulate the transcription of multiple genes in Cd stress response. • The Cd stress response of BpMYB1 involves in the gibberellin-dependant signaling. • BpMYB1 could recognize downstream genes of BpFC2 , BpbHLH93 , BpbZIP1 , BpbZIP-CPC1. • BpFC2 , BpbHLH93 , BpbZIP1 , BpbZIP-CPC1 overexpression improves plant Cd uptake. [ABSTRACT FROM AUTHOR]

The gut-brain axis is a crucial interface between the central nervous system and the gut microbiota. Recent evidence shows that exposure to environmental contaminants, such as heavy metals, can cause dysbiosis in gut microbiota, which may affect the gut-brain communication, impacting aspects of brain function and behavior. This systematic review of the literature aims to evaluate whether deleterious effects on brain function due to heavy metal exposure could be mediated by changes in the gut microbiota profile. Animal studies involving exposure to heavy metals and a comparison with a control group that evaluated neuropsychological outcomes and/or molecular outcomes along with the analysis of microbiota composition were reviewed. The authors independently assessed studies for inclusion, extracted data and assessed risk of bias using the protocol of Systematic Review Center for Laboratory Animal Experimentation (SYRCLE) for preclinical studies. A search in 3 databases yielded 16 eligible studies focused on lead (n = 10), cadmium (n = 1), mercury (n = 3), manganese (n = 1), and combined exposure of lead and manganese (n = 1). The animal species were rats (n = 7), mice (n = 4), zebrafish (n = 3), carp (n = 1) and fruit fly (n = 1). Heavy metals were found to adversely affect cognitive function, behavior, and neuronal morphology. Moreover, heavy metal exposure was associated with changes in the abundance of specific bacterial phyla, such as Firmicutes and Proteobacteria , which play crucial roles in gut health. In some studies, these alterations were correlated with learning and memory impairments and mood disorders. The interplay of heavy metals, gut microbiota, and brain suggests that heavy metals can induce direct brain alterations and indirect effects through the microbiota, contributing to neurotoxicity and the development of neuropsychological disorders. However, the small number of papers under review makes it difficult to draw definitive conclusions. Further research is warranted to unravel the underlying mechanisms and evaluate the translational implications for human health. [Display omitted] • This systematic review included 16 studies that exposed animals to Pb, Mn, Cd and Hg. • Heavy metal exposure affects gut microbiota, cognition, behavior & brain morphology. • Majors changes were in Firmicutes and Proteobacteria, albeit with conflicting results. • Gut dysbiosis due to heavy metals were correlated with mood and cognitive disorders. • Further research is essential to uncover mechanisms and health implications. [ABSTRACT FROM AUTHOR]

• Juveniles of sea bream Sparus aurata were exposed to cadmium chloride for up to 120 days. • The effects of the exposure were evaluated on the hepatopancreas architecture. • In a time-dependent manner, cadmium was absorbed and stored within the tissue. • Severe morphological and functional damages were detected. • Cadmium induced endocrine disrupting effect on parenchyma. In recent decades, cadmium has emerged as an environmental stressor in aquatic ecosystems due to its persistence and toxicity. It can enter water bodies from various natural and anthropogenic sources and, once introduced into aquatic systems, can accumulate in sediments and biota, leading to bioaccumulation and biomagnification in the food chain. For this reason, the effects of cadmium on aquatic life remain an area of ongoing research and concern. In this paper, a multidisciplinary approach was used to assess the effects of long-term exposure to an environmental concentration on the hepatopancreas of farmed juveniles of sea bream, Sparus aurata. After determining metal uptake, metallothionein production was assessed to gain insight into the organism's defence response. The effects were also assessed by histological and ultrastructural analyses. The results indicate that cadmium accumulates in the hepatopancreas at significant concentrations, inducing structural and functional damage. Despite the parallel increase in metallothioneins, fibrosis, alterations in carbohydrate distribution and endocrine disruption were also observed. These effects would decrease animal fitness although it did not translate into high mortality or reduced growth. This could depend on the fact that the animals were farmed, protected from the pressure deriving from having to search for food or escape from predators. Not to be underestimated is the return to humans, as this species is edible. Understanding the behaviour of cadmium in aquatic systems, its effects at different trophic levels and the potential risks to human health from the consumption of contaminated seafood would therefore be essential for informed environmental management and policy decisions. [ABSTRACT FROM AUTHOR]