scholarly journals Methionine synthase 1 provides methionine for activation of the GLR3.5 Ca2+ channel and regulation of germination in Arabidopsis

2019 ◽  
Vol 71 (1) ◽  
pp. 178-187 ◽  
Author(s):  
Chuanli Ju ◽  
Dongdong Kong ◽  
Yuree Lee ◽  
Gege Ge ◽  
Yanan Song ◽  
...  

Abstract Seed germination is a developmental process regulated by numerous internal and external cues. Our previous studies have shown that calcium influx mediated by the Arabidopsis glutamate receptor homolog 3.5 (AtGLR3.5) modulates the expression of the ABSCISIC ACID INSENSITIVE 4 (ABI4) transcription factor during germination and that L-methionine (L-Met) activates AtGLR3.1/3.5 Ca2+ channels in guard cells. However, it is not known whether L-Met participates in regulation of germination and what cellular mechanism is responsible for Met production during germination. Here, we describe Arabidopsis methionine synthase 1 (AtMS1), which acts in the final step of Met biosynthesis, synthesizes the Met required for the activation of AtGLR3.5 Ca2+ channels whose expression is up-regulated during germination, leading to the regulation of seed germination. We show that exogenous L-Met promotes germination in an AtGRL3.5-dependent manner. We also demonstrate that L-Met directly regulates the AtGLR3.5-mediated increase in cytosolic Ca2+ level in seedlings. We provide pharmacological and genetic evidence that Met synthesized via AtMS1 acts upstream of the AtGLR3.5-mediated Ca2+ signal and regulates the expression of ABI4, a major regulator in the abscisic acid response in seeds. Overall, our results link AtMS1, L-Met, the AtGLR3.5 Ca2+ channel, Ca2+ signals, and ABI4, and shed light on the physiological role and molecular mechanism of L-Met in germination.

Author(s):  
Haiyan Zhang ◽  
Liping Zhang ◽  
Yunrui Ji ◽  
Yifen Jing ◽  
Lanxin Li ◽  
...  

Abstract The plant-specific VQ gene family participates in diverse physiological processes but little information is available on their role in leaf senescence. Here, we show that the VQ motif-containing proteins, Arabidopsis SIGMA FACTOR BINDING PROTEIN1 (SIB1) and SIB2 are negative regulators of abscisic acid (ABA)-mediated leaf senescence. Loss of SIB1 and SIB2 function resulted in increased sensitivity of ABA-induced leaf senescence. In contrast, overexpression of SIB1 significantly delayed this process. Moreover, biochemical studies revealed that SIBs interact with WRKY75 transcription factor. Loss of WRKY75 function decreased sensitivity to ABA-induced leaf senescence, while overexpression of WRKY75 significantly accelerated this process. Chromatin immunoprecipitation assays revealed that WRKY75 directly binds to the promoters of GOLDEN 2-LIKE1(GLK1) and GLK2, to repress their expression. SIBs repress the transcriptional function of WRKY75 and negatively regulate ABA-induced leaf senescence in a WRKY75-dependent manner. In contrast, WRKY75 positively modulates ABA-mediated leaf senescence in a GLK-dependent manner. In addition, SIBs inhibit WRKY75 function in ABA-mediated seed germination. These results demonstrate that SIBs can form a complex with WRKY75 to regulate ABA-mediated leaf senescence and seed germination.


1997 ◽  
Vol 24 (6) ◽  
pp. 805 ◽  
Author(s):  
Robert J. Reid ◽  
Mark A. Tester ◽  
F. Andrew Smith

This work describes quantitative measurements of membrane fluxes of Ca2+ in intact cells of Chara corallina Klein ex Will. em. R.D. Wood, in relation to the control of Ca2+ uptake by membrane voltage (PD). At the normal resting PD, 45Ca influx was low but was stimulated up to 25-fold when the membrane was depolarised by voltage clamping to values more positive than –100 mV . Similarly, in cells in which the PD was varied by changing the concentration of K+ in the external solution, influx was strongly stimulated in the depolarised state. Transient depolarisation during action potentials resulted in large influxes of 45Ca which, when averaged over the duration of the action potential, yielded influxes of up to 2000 times higher than the resting level. Thus, there appears to be a large surplus of Ca2+ channels over that required for adequate nutrition. The possible physiological role of voltage-dependent Ca2+ channels is discussed in relation to the fact that, under normal growth conditions, cells of Chara corallina exist in the hyperpolarised state where these channels would not be activated.


Author(s):  
Faiza Bashir ◽  
Ateeq Ur Rehman ◽  
Milán Szabó ◽  
Imre Vass

AbstractSinglet oxygen (1O2) is an important damaging agent, which is produced during illumination by the interaction of the triplet excited state pigment molecules with molecular oxygen. In cells of photosynthetic organisms 1O2 is formed primarily in chlorophyll containing complexes, and damages pigments, lipids, proteins and other cellular constituents in their environment. A useful approach to study the physiological role of 1O2 is the utilization of external photosensitizers. In the present study, we employed a multiwell plate-based screening method in combination with chlorophyll fluorescence imaging to characterize the effect of externally produced 1O2 on the photosynthetic activity of isolated thylakoid membranes and intact Chlorella sorokiniana cells. The results show that the external 1O2 produced by the photosensitization reactions of Rose Bengal damages Photosystem II both in isolated thylakoid membranes and in intact cells in a concentration dependent manner indicating that 1O2 plays a significant role in photodamage of Photosystem II.


Cancers ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 533
Author(s):  
Rania F. Zaarour ◽  
Bilal Azakir ◽  
Edries Y. Hajam ◽  
Husam Nawafleh ◽  
Nagwa A. Zeinelabdin ◽  
...  

Programmed cell death or type I apoptosis has been extensively studied and its contribution to the pathogenesis of disease is well established. However, autophagy functions together with apoptosis to determine the overall fate of the cell. The cross talk between this active self-destruction process and apoptosis is quite complex and contradictory as well, but it is unquestionably decisive for cell survival or cell death. Autophagy can promote tumor suppression but also tumor growth by inducing cancer-cell development and proliferation. In this review, we will discuss how autophagy reprograms tumor cells in the context of tumor hypoxic stress. We will illustrate how autophagy acts as both a suppressor and a driver of tumorigenesis through tuning survival in a context dependent manner. We also shed light on the relationship between autophagy and immune response in this complex regulation. A better understanding of the autophagy mechanisms and pathways will undoubtedly ameliorate the design of therapeutics aimed at targeting autophagy for future cancer immunotherapies.


1986 ◽  
Vol 64 (8) ◽  
pp. 1633-1641 ◽  
Author(s):  
Parvaneh Rafiee ◽  
Christopher O. Matthews ◽  
Joseph C. Bagshaw ◽  
Thomas H. MacRae

Under normal conditions, an encysted Artemia embryo undergoes a developmental process that culminates in the gradual, uninterrupted emergence of the prenauplius from the cyst. The hatching membrane surrounding the emerged organism is then ruptured, usually beginning at the posterior end, and a motile nauplius is released. We have observed this process microscopically in the presence and absence of cadmium and report that cadmium disrupts Artemia development in a dose–dependent manner. At 0.1 μM, cadmium slows emergence but nauplii eventually resume rellatively normal development. Emergence and hatching are either delayed considerably or almost entirely prevented at 1 μM cadmium. Cadmium at 10 μM, completely arrests emergence but development continues at a reduced rate, eventually resulting in hatching of some organisms without need for complete emergence. If organisms exposed to 10 μM cadmium are washed, abnormally shaped emerged forms are released and many of these eventually hatch, although in an unusual manner. Cadmium at 10 μM causes complete, rapid precipitation of purified Artemia tubulin at 0 °C but cadmium at the lower concentrations tested has no apparent inhibitory effect on microtubule assembly. Although we do not know the actual cadmium–induced physiological changes that result in abnormal development of Artemia, our results indicate that we can now examine the interdependence of morphological and molecular aspects of Artemia development in a way not previously possible.


Planta ◽  
2004 ◽  
Vol 220 (2) ◽  
pp. 251-261 ◽  
Author(s):  
E. A. Amaral da Silva ◽  
Peter E. Toorop ◽  
Adriaan C. van Aelst ◽  
Henk W. M. Hilhorst

1992 ◽  
Vol 70 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Maria Touraki ◽  
Antigone Lazou

The effect of adenosine on the calcium paradox in the isolated frog heart was studied. Addition of adenosine during calcium depletion protected the frog heart against a calcium paradox. This protective effect was indicated by reduced protein and creatine kinase release, maintenance of electrical activity, and recovery of mechanical activity during reperfusion. Tissue calcium determination results showed that adenosine protected frog myocardial cells by reducing the massive calcium influx during reperfusion possibly through an action on calcium channels. Adenosine exerted its action in a dose-dependent manner; a concentration of 10 μM adenosine provided maximum protection of myocardial cells against the calcium paradox damage. Higher concentrations of adenosine produced side effects on both electrical and mechanical activity. These results are discussed in terms of the possible mechanism involved in the protective effect of adenosine.Key words: calcium paradox, adenosine, frog heart.


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