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Atrazine (ATR) is one of the herbicides widely used worldwide. Meanwhile, it is an environmental endocrine disruptor that can cross the blood-brain barrier and cause damage to the endocrine-nervous system, especially by affecting the normal secretion of dopamine (DA). Regrettably, effector markers and cascade response mechanisms in damaged dopaminergic neurons induced by ATR exposure remain elusive. In this paper, we focus on investigating aggregation and position change of transactive response DNA-binding protein-43 (TDP-43) after ATR exposure, and illustrating whether TDP-43 can serve as a potential marker of mitochondrial dysfunction which causes damage to dopaminergic neurons. In our study, we used rat adrenal pheochromocytoma cell line 12 (PC12) to establish an in vitro model of dopaminergic neurons. After PC12 was intervened by ATR, we found reduced DA cycling and DA levels, and that TDP-43 aggregated continuously in the cytoplasm and then translocated to mitochondria. Furthermore, the studies we have performed showed that the translocation can cause mitochondrial dysfunction through activating the unfolded mitochondrial protein response (UPRmt), ultimately causing damage to dopaminergic neuron. The research we have done suggests that TDP-43 can serve as a potential effector marker of dopaminergic neuron damaged caused by ATR exposure.

Plasmopara halstedii (Farl.) Berl. & De Toni causing downy mildew of sunflower is responsible for considerable economic losses worldwide. Because P. halstedii can be seed-transmitted, monitoring of seeds for pathogen contamination is important for the sunflower seed trade. The relevance of asymptomatic or latent infections as factors of disease spread have not been studied by molecular techniques. A molecular marker based on a putative effector gene of P. halstedii was used to examine the pathogen’s presence in asymptomatic sunflowers growing near patches of mildewed plants in naturally infected fields. The method based on conventional PCR was highly sensitive for detection of P. halstedii in DNA from whole seeds. By the application of this protocol, we found that all seed samples obtained from symptomatic plants amplified the expected fragment, whereas the diagnostic marker identified the presence of pathogen in one out of 21 asymptomatic plants. Possible uses of this marker to detect downy mildew in seed from asymptomatic plants or for race identification are discussed.

Plasmopara halstedii (Farl.) Berl. & De Toni causing downy mildew of sunflower is responsible for considerable economic losses worldwide. Because P. halstedii can be seed-transmitted, monitoring of seeds for pathogen contamination is important for the sunflower seed trade. The relevance of asymptomatic or latent infections as factors of disease spread have not been studied by molecular techniques. A molecular marker based on a putative effector gene of P. halstedii was used to examine the pathogen's presence in asymptomatic sunflowers growing near patches of mildewed plants in naturally infected fields. The method based on conventional PCR was highly sensitive for detection of P. halstedii in DNA from whole seeds. By the application of this protocol, we found that all seed samples obtained from symptomatic plants amplified the expected fragment, whereas the diagnostic marker identified the presence of pathogen in one out of 21 asymptomatic plants. Possible uses of this marker to detect downy mildew in seed from asymptomatic plants or for race identification are discussed. [ABSTRACT FROM AUTHOR]

Atrazine (ATR) is one of the herbicides widely used worldwide. Meanwhile, it is an environmental endocrine disruptor that can cross the blood-brain barrier and cause damage to the endocrine-nervous system, especially by affecting the normal secretion of dopamine (DA). Regrettably, effector markers and cascade response mechanisms in damaged dopaminergic neurons induced by ATR exposure remain elusive. In this paper, we focus on investigating aggregation and position change of transactive response DNA-binding protein-43 (TDP-43) after ATR exposure, and illustrating whether TDP-43 can serve as a potential marker of mitochondrial dysfunction which causes damage to dopaminergic neurons. In our study, we used rat adrenal pheochromocytoma cell line 12 (PC12) to establish an in vitro model of dopaminergic neurons. After PC12 was intervened by ATR, we found reduced DA cycling and DA levels, and that TDP-43 aggregated continuously in the cytoplasm and then translocated to mitochondria. Furthermore, the studies we have performed showed that the translocation can cause mitochondrial dysfunction through activating the unfolded mitochondrial protein response (UPRmt), ultimately causing damage to dopaminergic neuron. The research we have done suggests that TDP-43 can serve as a potential effector marker of dopaminergic neuron damaged caused by ATR exposure. • TDP-43 is a potential effector marker of dopaminergic neuronal damaged caused by ATR exposure. • Translocation and importation of TDP-43 can cause mitochondrial dysfunction. • UPRmt plays a dual role in TDP-43-induced mitochondrial disorders. [ABSTRACT FROM AUTHOR]