Browsing by Author "Mwimba, Musoki"
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Item Open Access Circadian Regulation of Plant Physiology: A New Role for Humidity, the Forgotten Zeitgeber(2016) Mwimba, MusokiAir humidity is an environmental cue that influences many physiological responses in terrestrial organisms. In early chronobiology studies, it was thought that humidity could influence the circadian clock. However, no further studies have been performed in pursuit of this idea, nor humidity been investigated as a potential Zeitgeber, despite the fact that daily humidity fluctuation has been widely observed. Here, we report that humidity is a Zeitgeber on par with light and temperature and that it can fundamentally influence plant physiology. Using 10 years of weather records obtained from Harvard Forest and Weather Underground databases, we quantitatively characterized humidity oscillation as a natural phenomenon and found that the circadian oscillation of humidity (i.e., lower during the day and higher at night) is robust and independent of climates or seasons. Moreover, there is a 2-hour overlap of high humidity with light in the morning, suggesting a possible interplay between these two environmental cues and the circadian clock. We then tested and found that humidity can indeed entrain the circadian clock as a bona fide Zeitgeber through regulation of the plant core morning clock gene CCA1 (CIRCADIAN CLOCK ASSOCIATED 1) and the core evening clock gene TOC1 (TIMING OF CAB EXPRESSION 1). However, the core morning clock gene LHY (LATE ELONGATED HYPOCOTYL), partner of CCA1, resists the humidity-entrainment, indicating that the plant circadian clock may have two intertwined loops: one is responsive to both light and humidity via CCA1, whereas the other is responsive only to light mediated by LHY. In the absence of rhythmic light signal, humidity can entrain the clock, whereas in the presence of light in the morning, humidity synergistically reinforces the clock. At the physiological level, the humidity-entrained clock provides additional advantages to plants. It can improve energy storage, reduce the flowering time and improve seed production in a circadian-dependent manner. Additionally, we found that humidity can fundamentally shape plant-microbe interactions because it is a key signal for the initial induction of the bacterial type III secretion system and effector genes required for virulence. Thus, it is necessary for plants to mount an appropriate response to pathogen infections at night when humidity naturally rises. These findings demonstrate how terrestrial organisms could adapt to humidity oscillation, a universal environmental cue, to strategically maximize their own fitness. We propose that humidity-sensing might be an ancient determinant shaping the evolution of terrestrial organisms after their transition away from aquatic environment.
Item Open Access H2O2 sulfenylates CHE linking local infection to establishment of systemic acquired resistance.(bioRxiv, 2023-08-01) Cao, Lijun; Yoo, Heejin; Chen, Tianyuan; Mwimba, Musoki; Zhang, Xing; Dong, XinnianIn plants, a local infection can lead to systemic acquired resistance (SAR) through increased production of salicylic acid (SA). For 30 years, the identity of the mobile signal and its direct transduction mechanism for systemic SA synthesis in initiating SAR have been hotly debated. We found that, upon pathogen challenge, the cysteine residue of transcription factor CHE undergoes sulfenylation in systemic tissues, enhancing its binding to the promoter of SA-synthesis gene, ICS1, and increasing SA production. This occurs independently of previously reported pipecolic acid (Pip) signal. Instead, H2O2 produced by NADPH oxidase, RBOHD, is the mobile signal that sulfenylates CHE in a concentration-dependent manner. This modification serves as a molecular switch that activates CHE-mediated SA-increase and subsequent Pip-accumulation in systemic tissues to synergistically induce SAR.Item Open Access Quantification of the humidity effect on HR by Ion leakage assay.(Bio-protocol, 2019-04-05) Mwimba, Musoki; Dong, XinnianWe describe a protocol to measure the contribution of humidity on cell death during the effector-triggered immunity (ETI), the plant immune response triggered by the recognition of pathogen effectors by plant resistance genes. This protocol quantifies tissue cell death by measuring ion leakage due to loss of membrane integrity during the hypersensitive response (HR), the ETI-associated cell death. The method is simple and short enough to handle many biological replicates, which improves the power of test of statistical significance. The protocol is easily applicable to other environmental cues, such as light and temperature, or treatment with chemicals.Item Open Access Salicylic acid receptors activate jasmonic acid signalling through a non-canonical pathway to promote effector-triggered immunity.(Nature communications, 2016-10-11) Liu, Lijing; Sonbol, Fathi-Mohamed; Huot, Bethany; Gu, Yangnan; Withers, John; Mwimba, Musoki; Yao, Jian; He, Sheng Yang; Dong, XinnianIt is an apparent conundrum how plants evolved effector-triggered immunity (ETI), involving programmed cell death (PCD), as a major defence mechanism against biotrophic pathogens, because ETI-associated PCD could leave them vulnerable to necrotrophic pathogens that thrive on dead host cells. Interestingly, during ETI, the normally antagonistic defence hormones, salicylic acid (SA) and jasmonic acid (JA) associated with defence against biotrophs and necrotrophs respectively, both accumulate to high levels. In this study, we made the surprising finding that JA is a positive regulator of RPS2-mediated ETI. Early induction of JA-responsive genes and de novo JA synthesis following SA accumulation is activated through the SA receptors NPR3 and NPR4, instead of the JA receptor COI1. We provide evidence that NPR3 and NPR4 may mediate this effect by promoting degradation of the JA transcriptional repressor JAZs. This unique interplay between SA and JA offers a possible explanation of how plants can mount defence against a biotrophic pathogen without becoming vulnerable to necrotrophic pathogens.