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The Ca²⁺-CaM Signaling Pathway Mediates Potassium Uptake by Regulating Reactive Oxygen Species Homeostasis in Tobacco Roots Under Low-K⁺ Stress.

ABSTRACT: Potassium (K⁺) deficiency severely threatens crop growth and productivity. Calcium (Ca²⁺) signaling and its sensors play a central role in the response to low-K⁺ stress. Calmodulin (CaM) is an important Ca²⁺ sensor. However, the mechanism by which Ca²⁺ signaling and CaM mediate the response of roots to low-K⁺ stress remains unclear. In this study, we found that the K⁺ concentration significantly decreased in both shoots and roots treated with Ca²⁺ channel blockers, a Ca²⁺ chelator, and CaM antagonists. Under low-K⁺ stress, reactive oxygen species (ROS) accumulated, and the activity of antioxidant enzymes, NAD kinase (NADK), and NADP phosphatase (NADPase) decreased. This indicates that antioxidant enzymes, NADK, and NADPase might be downstream target proteins in the Ca²⁺-CaM signaling pathway, which facilitates K⁺ uptake in plant roots by mediating ROS homeostasis under low-K⁺ stress. Moreover, the expression of NtCNGC3, NtCNGC10, K⁺ channel genes, and transporter genes was significantly downregulated in blocker-treated, chelator-treated, and antagonist-treated plant roots in the low K⁺ treatment, suggesting that the Ca²⁺-CaM signaling pathway may mediate K⁺ uptake by regulating the expression of these genes. Overall, this study shows that the Ca²⁺-CaM signaling pathway promotes K⁺ absorption by regulating ROS homeostasis and the expression of K⁺ uptake-related genes in plant roots under low-K⁺ stress.

SUBMITTER: Wang Y

PROVIDER: S-EPMC8216240 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Mechanical forces from non-ablative pulsed focused ultrasound (pFUS) generate pro-inflammatory tumor microenvironments (TME), marked by increased cytokines, chemokines, and trophic factors, as well as immune cell infiltration and reduced tumor growth. pFUS also causes DNA damage within tumors, which is a potent activator of immunity and could contribute to changes in the TME. This study investigated mechanisms behind the mechanotransductive effects of pFUS causing DNA damage in several tumor cell types. Methods: 4T1 (murine breast tumor), B16 (murine melanoma), C6 (rat glioma), or MDA-MB-231 (human breast tumor) cells were sonicated in vitro (1.1MHz; 6MPa PNP; 10ms pulses; 10% duty cycle; 300 pulses). DNA damage was detected by TUNEL, apoptosis was measured by immunocytochemistry for cleaved caspase-3. Calcium, superoxide, and H2O2 were detected by fluorescent indicators and modulated by BAPTA-AM, mtTEMPOL, or Trolox, respectively. Results: pFUS increased TUNEL reactivity (range = 1.6-2.7-fold) in all cell types except C6 and did not induce apoptosis in any cell line. All lines displayed cytosolic Ca2+ transients during sonication. pFUS increased superoxide (range = 1.6-2.0-fold) and H2O2 (range = 2.3-2.8-fold) in all cell types except C6. BAPTA-AM blocked increased TUNEL reactivity, superoxide and H2O2 formation, while Trolox also blocked increased TUNEL reactivity increased after pFUS. mtTEMPOL allowed H2O2 formation and did not block increased TUNEL reactivity after pFUS. Unsonicated C6 cells had higher baseline concentrations of cytosolic Ca2+, superoxide, and H2O2, which were not associated with greater baseline TUNEL reactivity than the other cell lines. Conclusions: Mechanotransduction of pFUS directly induces DNA damage in tumor cells by cytosolic Ca2+ transients causing formation of superoxide and subsequently, H2O2. These results further suggest potential clinical utility for pFUS. However, the lack of pFUS-induced DNA damage in C6 cells demonstrates a range of potential tumor responses that may arise from physiological differences such as Ca2+ or redox homeostasis.

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The Ca²⁺-CaM Signaling Pathway Mediates Potassium Uptake by Regulating Reactive Oxygen Species Homeostasis in Tobacco Roots Under Low-K⁺ Stress.

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The Ca2+-CaM Signaling Pathway Mediates Potassium Uptake by Regulating Reactive Oxygen Species Homeostasis in Tobacco Roots Under Low-K+ Stress.

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OmicsDI is part of the ELIXIR infrastructure

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The Ca²⁺-CaM Signaling Pathway Mediates Potassium Uptake by Regulating Reactive Oxygen Species Homeostasis in Tobacco Roots Under Low-K⁺ Stress.