CqZF-HD14 enhances drought tolerance in quinoa seedlings through interaction with CqHIPP34 and CqNAC79.

Drought stress is a key agricultural problem that restricts plant development and crop yield. Research on quinoa (Chenopodium quinoa), a nutrient-rich crop with strong stress resistance, has been limited in terms of the molecular regulation of its adaptation to drought stress. This study identified the zinc finger-homeodomain (ZF-HD) family in quinoa and a drought-responsive Chenopodium quinoa ZF-HD14 (CqZF-HD14) through expression profiles. Transient overexpression of CqZF-HD14 promotes photosynthetic pigment accumulation under drought stress, strengthens the antioxidant system, and in turn enhances drought tolerance. Comprehensive genome-wide family analysis and expression profiling identified CqNAC79 and CqHIPP34 regulated by CqZF-HD14, and their interactions were further determined by bimolecular fluorescence complementation (BIFC). Moreover, physiological and biochemical analyses and transient overexpression also revealed that CqNAC79 and CqHIPP34 resist drought by promoting the accumulation of photosynthetic pigments and maintaining antioxidant capacity under drought stress. The synergistic effect of CqZF-HD14 with CqNAC79 or CqHIPP34 further enhanced the drought tolerance of quinoa seedlings. Taken together, the results indicate that CqZF-HD14, CqNAC79 and CqHIPP34 may be important contributors to the drought tolerance regulatory network in quinoa, and these findings add new members to the drought tolerance gene pool.

Malate-mediated CqMADS68 enhances aluminum tolerance in quinoa seedlings through interaction with CqSTOP6, CqALMT6 and CqWRKY88.

Aluminum (Al) stress in acidic soils has severe negative effects on crop productivity. In this study, the alleviating effect and related mechanism of malate on Al stress in quinoa (Chenopodium quinoa) seedlings were investigated. The findings indicated that malate alleviated the growth inhibition of quinoa seedlings under Al stress, maintained the enzymatic and nonenzymatic antioxidant systems, and aided resistance to the damage caused by excessive reactive oxygen species (ROS). Under Al stress, malate significantly increased the contents of chlorophyll and carotenoids in quinoa shoots by 103.8% and 240.7%, and significantly increased the ratios of glutathione (GSH)/oxidized glutathione (GSSG), and ascorbate (AsA)/dehydroascorbate (DHA) in roots by 59.9% and 699.2%, respectively. However, malate significantly decreased the superoxide radical (O2•-), hydrogen peroxide (H2O2), malondialdehyde (MDA) and Al contents in quinoa roots under Al stress by 32.7%, 60.9%, 63.1% and 49%, respectively. Moreover, the CqMADS family and the Al stress-responsive gene families (CqSTOP, CqALMT, and CqWRKY) were identified from the quinoa genome. Comprehensive expression profiling identified CqMADS68 as being involved in malate-mediated Al resistance. Transient overexpression of CqMADS68 increased Al tolerance in quinoa seedlings. More importantly, we found that CqMADS68 regulated the expression of CqSTOP6, CqALMT6 and CqWRKY88 and further demonstrated the interaction of CqMADS68 with CqSTOP6, CqALMT6 and CqWRKY88 by bimolecular fluorescence complementation (BIFC) experiments. Moreover, transient overexpression and physiological and biochemical analyses demonstrated that CqSTOP6, CqALMT6 and CqWRKY88 could also improve Al tolerance by maintaining the antioxidant capacity of quinoa seedlings. Taken together, these findings reveal that CqMADS68, CqSTOP6, CqALMT6 and CqWRKY88 may be important contributors to the Al tolerance regulatory network in quinoa, providing new insights into Al stress resistance.

Involvement of several putative transporters of different families in ß-cyclocitral-induced alleviation of cadmium toxicity in quinoa (Chenopodium quinoa) seedlings.

Cadmium (Cd) has a serious negative impact on crop growth and human food security. This study investigated the alleviating effect of ß-cyclocitral, a potential heavy metal barrier, on Cd stress in quinoa seedlings and the associated mechanisms. Our results showed that ß-cyclocitral alleviated Cd stress-induced growth inhibition in quinoa seedlings and promoted quinoa seedling root development under Cd stress. Moreover, it maintained the antioxidant system of quinoa seedlings, including the enzymatic, i.e., superoxide dismutase (SOD), peroxidase (POD), catalase (CAT), ascorbate peroxidase (APX), and nonenzymatic, i.e., reduced glutathione (GSH) and ascorbic acid (ASA), antioxidants, which eliminate the damage from excessive reactive oxygen species (ROS). Our results showed that ß-cyclocitral could reduce the amount of Cd absorbed by roots. Furthermore, we systematically identified five transporter families from the quinoa genome, and the RT-qPCR results showed that ZIP, Nramp and YSL gene families were downregulated by ß-cyclocitral to reduce Cd uptake by roots. Thus, ß-cyclocitral promoted the growth, photosynthetic capacity and antioxidant capacity of the aboveground parts of quinoa seedlings. Taken together, these results suggested that the ß-cyclocitral-induced decrease in Cd uptake may be caused by the downregulation of several selected transporter genes.