Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008272 (chlorosis)
 2,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The tobacco gene NtWIN4 (Nicotiana tabacum wound-induced clone 4) is transiently up-regulated in response not only to wounding but also to pathogen attack. NtWIN4 encodes a putative basic helix-loop-helix protein with an apparent molecular mass of 28 kDa that exhibited clear nuclear transcription repression activity in Dual-Luciferase assays. However, immunoblotting indicated the existence of a 17-kDa form of NtWIN4 localized exclusively in tobacco leaf chloroplasts. Subsequent peptide dissection analyses with green fluorescent protein fusions revealed that a polypeptide of 81 amino acids starting at position 13 from the N terminus is maximally necessary for this localization. Further fine dissection analysis strongly suggested that the protein actually begins at the second Met located at position 27, yielding a signal peptide of 67 amino acids. However, the last C-terminal 15 amino acids overlap with the conserved basic region critical for DNA binding, so NtWIN4 presumably does not function as a transcription factor in planta. Transgenic tobacco plants constitutively overexpressing NtWIN4 demonstrated mortality with abnormal features, including albinism, and transient expression upon agroinfiltration resulted in distinct necrosis with a sharp decrease in chlorophyll content, consistent with the phenomenon known as chlorosis. Transgenic RNA interference tobacco plants exhibited reduced hypersensitive cell death, showing delayed tissue necrosis upon pathogen infection. These results suggest that NtWIN4 arose by divergence, becoming a chloroplast-resident factor from a nuclear transcriptional repressor by obtaining a transit peptide sequence, and that, upon translocation, it interacts with chloroplast components to induce hypersensitive cell death through chloroplast disruption, thereby contributing to plant stress responses.
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PMID:Evolution of a basic helix-loop-helix protein from a transcriptional repressor to a plastid-resident regulatory factor: involvement in hypersensitive cell death in tobacco plants. 1696 34

Cadmium (Cd) is toxic to plant cells. Under Cd exposure, the plant displayed leaf chlorosis, which is a typical symptom of iron (Fe) deficiency. Interactions of Cd with Fe have been reported. However, the molecular mechanisms of Cd-Fe interactions are not well understood. Here, we showed that FER-like Deficiency Induced Transcripition Factor (FIT), AtbHLH38, and AtbHLH39, three basic helix-loop-helix transcription factors involved in Fe homeostasis in plants, also play important roles in Cd tolerance. The gene expression analysis showed that the expression of FIT, AtbHLH38, and AtbHLH39 was up-regulated in the roots of plants treated with Cd. The plants overexpressing AtbHLH39 and double-overexpressing FIT/AtbHLH38 and FIT/AtbHLH39 exhibited more tolerance to Cd exposure than wild type, whereas no Cd tolerance was observed in plants overexpressing either AtbHLH38 or FIT. Further analysis revealed that co-overexpression of FIT with AtbHLH38 or AtbHLH39 constitutively activated the expression of Heavy Metal Associated3 (HMA3), Metal Tolerance Protein3 (MTP3), Iron Regulated Transporter2 (IRT2), and Iron Regulated Gene2 (IREG2), which are involved in the heavy metal detoxification in Arabidopsis (Arabidopis thaliana). Moreover, co-overexpression of FIT with AtbHLH38 or AtbHLH39 also enhanced the expression of NICOTIANAMINE SYNTHETASE1 (NAS1) and NAS2, resulting in the accumulation of nicotiananamine, a crucial chelator for Fe transportation and homeostasis. Finally, we showed that maintaining high Fe content in shoots under Cd exposure could alleviate the Cd toxicity. Our results provide new insight to understand the molecular mechanisms of Cd tolerance in plants.
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PMID:Co-overexpression FIT with AtbHLH38 or AtbHLH39 in Arabidopsis-enhanced cadmium tolerance via increased cadmium sequestration in roots and improved iron homeostasis of shoots. 2218 55

Iron (Fe) is essential for plant growth and development. Knowledge of Fe signaling, from the beginning of perception to activation of the uptake process, is critical for crop improvement. Here, by using chemical screening, we identified a small molecule 3-amino-N-(3-methylphenyl)thieno[2,3-b]pyridine-2-carboxamide named R7 ('R' denoting repressor of IRON-REGULATED TRANSPORTER 1), that modulates Fe homeostasis of Arabidopsis. R7 treatment led to reduced Fe levels in plants, thus causing severe chlorosis under Fe deficiency. Expression analysis of central transcription factors, FER-LIKE IRON DEFICIENCY INDUCED TRANSCRIPTION FACTOR (FIT) and subgroup Ib basic helix-loop-helix (Ib bHLH) genes bHLH38/39/100/101, revealed that R7 targets the FIT-dependent transcriptional pathway. Exogenously supplying S-nitrosoglutathione (GSNO), but not other nitric oxide (NO) donors sodium nitroprusside (SNP) and S-nitroso-N-acetyl-dl-penicillamine (SANP), alleviated the inhibitory effects of R7 on Fe homeostasis. R7 did not inhibit cellular levels of NO or glutathione but decreased GSNO level in roots. We demonstrate that NO is involved in regulating not only the FIT transcriptional network but also the Ib bHLH networks. In addition, GSNO, from S-nitrosylation of glutathione, specifically mediates the Fe-starvation signal to FIT, which is distinct from the NO to Ib bHLH signal. Our work dissects the molecular connection between NO and the Fe-starvation response. We present a new signaling route whereby GSNO acts downstream of NO to trigger the Fe-deficiency response in Arabidopsis.
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PMID:S-Nitrosoglutathione works downstream of nitric oxide to mediate iron-deficiency signaling in Arabidopsis. 2939 86

Iron is an indispensable micronutrient for plant growth and development. Limited bioavailability of Fe in the soil leads to iron deficiency chlorosis in plants and yield loss. In this study, two soybean basic helix-loop-helix transcription factors, GmbHLH57 and GmbHLH300, were identified in response to Fe-deficiency. Both transcription factors are expressed in roots and nodules, and are induced by Fe deficiency; these patterns were confirmed in transgenic hairy roots expressing constructs of the endogenous promoters fused to a GUS reporter gene. Bimolecular fluorescence complementation, yeast two-hybrid and coimmunoprecipitation (co-IP) assays indicated a physical interaction between GmbHLH57 and GmbHLH300. Studies on transgenic soybeans overexpressing GmbHLH57 and GmbHLH300 revealed that overexpression of each transcription factor, alone, results in no change of the responses to Fe deficiency, whereas overexpression of both transcription factors upregulated the downstream Fe uptake genes and increased the Fe content in these transgenic plants. Compared to wild type, these double overexpression transgenic plants were more tolerant to Fe deficiency. Taken together, our findings establish that GmbHLH57 and GmbHLH300 are important transcription factors involved in Fe homeostasis in soybean.
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PMID:Two soybean bHLH factors regulate response to iron deficiency. 2957 45

Plant growth requires optimal levels of iron (Fe). Fe is used for energy production, numerous enzymatic processes, and is indispensable for cellular metabolism. Recent studies have established the mechanism involved in Fe uptake and transport. However, our knowledge of Fe sensing and signaling is limited. Dissecting Fe signaling may be useful for crop improvement by Fe fortification. Here, we report two small-molecules, R3 and R6 [where R denotes repressor of IRON-REGULATED TRANSPORTER 1 (IRT1)], identified through a chemical screening, whose use blocked activation of the Fe-deficiency response in Arabidopsis thaliana. Physiological analysis of plants treated with R3 and R6 showed that these small molecules drastically attenuated the plant response to Fe starvation. Small-molecule treatment caused severe chlorosis and strongly reduced chlorophyll levels in plants. Fe content in shoots was decreased considerably by small-molecule treatments especially in Fe deficiency. Small-molecule treatments attenuated the Fe-deficiency-induced expression of the Fe uptake gene IRT1. Analysis of FER-LIKE IRON-DEFICIENCY-INDUCED TRANSCRIPTION FACTOR (FIT) and subgroup Ib basic helix-loop-helix (bHLH) gene (bHLH38/39/100/101) expression showed that R3 affects the FIT-network, whereas R6 affects both the FIT and Ib bHLH networks. An assessment of the effects of the structural analogs of R3 and R6 on the induction of Fe-dependent chlorosis revealed the functional motif of the investigated chemicals. Our findings suggest that small-molecules selectively modulate the distinct signaling routes that operate in response to Fe-deficiency. R3 and R6 likely interrupt the activity of key upstream signaling regulators whose activities are required for the activation of the Fe-starvation transcriptional cascade in Arabidopsis roots.
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PMID:Small-Molecules Selectively Modulate Iron-Deficiency Signaling Networks in Arabidopsis. 3076 41

Powdery mildew (PM), caused by Podosphaera xanthii, is a major threat to the global cucurbit yield. The molecular mechanisms underlying the PM resistance of pumpkin (Cucurbita moschata Duch.) are largely unknown. A homolog of the basic helix-loop-helix (bHLH) transcription factor was previously identified through a transcriptomic analysis of a PM-resistant pumpkin. In this study, this bHLH homolog in pumpkin has been functionally characterized. CmbHLH87 is present in the nucleus. CmbHLH87 expression in the PM-resistant material was considerably downregulated by PM; and abscisic acid, methyl jasmonate, ethephon, and NaCl treatments induced CmbHLH87 expression. Ectopic expression of CmbHLH87 in tobacco plants alleviated the PM symptoms on the leaves, accelerated cell necrosis, and enhanced H2O2 accumulation. The expression levels of PR1a, PR5, and NPR1 were higher in the PM-infected transgenic plants than in PM-infected wild-type plants. Additionally, the chlorosis and yellowing of plant materials were less extensive and the concentration of bacteria at infection sites was lower in the transgenic tobacco plants than in the wild-type plants in response to bacterial wilt and scab pathogens. CmbHLH87 may be useful for genetic engineering of novel pumpkin cultivars in the future.
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PMID:Expression of Pumpkin CmbHLH87 Gene Improves Powdery Mildew Resistance in Tobacco. 3231 77