Hypothesis: versatile function of ferredoxin-NADP+ reductase in cyanobacteria provides regulation for transient photosystem I-driven cyclic electron flow

2002 ◽  
Vol 29 (3) ◽  
pp. 201 ◽  
Author(s):  
Hans C. P. Matthijs ◽  
Robert Jeanjean ◽  
Nataliya Yeremenko ◽  
Jef Huisman ◽  
Francoise Joset ◽  
...  
Keyword(s):  
Electron Transfer ◽  
Salt Stress ◽  
De Novo ◽  
Electron Flow ◽  
High Co2 ◽  
Partial Restoration ◽  
Synechocystis Pcc6803 ◽  
Low Co2 ◽  
Cyclic Electron Transfer

Pseudo-reversion of the high-CO2 requiring phenotype of the NADH dehydrogenase type 1-impaired mutant of Synechocystis PCC6803, strain M55, by salt stress coincides with partial restoration of PSI-driven cyclic electron transfer. In M55, the complete family of D proteins (D1–D6) that are needed for electron transfer through the complex is lacking. Adaptation to salt stress requires de novo synthesis of full-length 47-kDa ferredoxin-NADP+ reductase (FNR). A mutant created in the M55 background, which only expresses truncated chloroplast 37-kDa FNR cannot adapt to salt stress and refrains from growth in low CO2. A special feature of FNR in cyanobacteria is the relatively high molecular mass of 44–48 kDa. A positively charged extended N-terminal domain of the cyanobacterial enzyme defines the extra mass. The extension likely plays a key role in the salt-stress inducible enhancement of PSI-driven cyclic electron transfer, and in the pseudo-reversion of the high-CO2 requiring phenotype of M55. Data acquired with several other cyanobacteria and the oxychlorobacterium Prochlorothrix hollandica contributed to the present hypothesis. It proposes that FNR is involved in regulation of inducible and transient PSI cyclic electron transfer in cyanobacteria via a thylakoid surface charge and conditional-proteolysis steered mechanism.

scholarly journals Feedback limitation of photosynthesis at high CO2 acts by modulating the activity of the chloroplast ATP synthase

2009 ◽  
Vol 36 (11) ◽  
pp. 893 ◽  
Author(s):  
Olavi Kiirats ◽  
Jeffrey A. Cruz ◽  
Gerald E. Edwards ◽  
David M. Kramer
Keyword(s):  
Electron Transfer ◽  
Atp Synthase ◽  
Atp Synthesis ◽  
Nicotiana Sylvestris ◽  
O2 Evolution ◽  
High Co2 ◽  
Chloroplast Atp Synthase ◽  
Low Co2 ◽  
Photosynthetic Electron Transfer

It was previously shown that photosynthetic electron transfer is controlled under low CO2 via regulation of the chloroplast ATP synthase. In the current work, we studied the regulation of photosynthesis under feedback limiting conditions, where photosynthesis is limited by the capacity to utilise triose-phosphate for synthesis of end products (starch or sucrose), in a starch-deficient mutant of Nicotiana sylvestris Speg. & Comes. At high CO2, we observed feedback control that was progressively reversed by increasing O2 levels from 2 to 40%. The activity of the ATP synthase, probed in vivo by the dark-interval relaxation kinetics of the electrochromic shift, was proportional to the O2-induced increases in O2 evolution from PSII (JO2), as well as the sum of Rubisco oxygenation (vo) and carboxylation (vc) rates. The altered ATP synthase activity led to changes in the light-driven proton motive force, resulting in regulation of the rate of plastoquinol oxidation at the cytochrome b6f complex, quantitatively accounting for the observed control of photosynthetic electron transfer. The ATP content of the cell decreases under feedback limitation, suggesting that the ATP synthesis was downregulated to a larger extent than ATP consumption. This likely resulted in slowing of ribulose bisphosphate regeneration and JO2). Overall, our results indicate that, just as at low CO2, feedback limitations control the light reactions of photosynthesis via regulation of the ATP synthase, and can be reconciled with regulation via stromal Pi, or an unknown allosteric affector.

Photosynthetic Control in Chloroplasts Suspensions Frozen in Liquid Nitrogen in the Presence of Glycerol

1977 ◽  
Vol 32 (3-4) ◽  
pp. 254-256 ◽  
Author(s):  
K. Kaminski
Keyword(s):  
Electron Transfer ◽  
Liquid Nitrogen ◽  
Electron Flow ◽  
Type A ◽  
Freezing And Thawing ◽  
Spinach Chloroplasts ◽  
Relative Decrease ◽  
Photosynthetic Control ◽  
Cyclic Electron Transfer

Abstract Type A complete spinach chloroplasts (photosynthetic control ratio ≅ 5) were frozen in liquid nitrogen, in the presence or absence of 50 percent glycerol (v/v). By considering five parameters related to the non cyclic electron transfer in the light (oxidant : K-ferricyanide) it was shown that the uncoupling due to freezing and thawing was partially prevented by glycerol. However glycerol was responsible for a slight uncoupling in fresh chloroplasts. The clearest uncoupling effect of freezing, and chiefly of glycerol, concerned the inhibition of the electron flow which follows the stimulation caused by a limiting quantity of ADP (state 4). The relative decrease of the photosynthetic control and of related parameters due to the use of this method of preservation, has to be balanced with the improved homogeneity and convenience resulting from it.

scholarly journals Mononuclear Phagocyte Differentiation, Activation, and Viral Infection Regulate Matrix Metalloproteinase Expression: Implications for Human Immunodeficiency Virus Type 1-Associated Dementia

2001 ◽  
Vol 75 (14) ◽  
pp. 6572-6583 ◽  
Author(s):  
Anuja Ghorpade ◽  
Raisa Persidskaia ◽  
Radhika Suryadevara ◽  
Myhanh Che ◽  
Xiao Juan Liu ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Viral Infection ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
De Novo ◽  
Mononuclear Phagocyte ◽  
Monocyte Migration ◽  
Immunodeficiency Virus ◽  
Hiv 1

ABSTRACT The pathogenesis of human immunodeficiency virus type 1 (HIV-1)-associated dementia (HAD) is mediated mainly by mononuclear phagocyte (MP) secretory products and their interactions with neural cells. Viral infection and MP immune activation may affect leukocyte entry into the brain. One factor that influences central nervous system (CNS) monocyte migration is matrix metalloproteinases (MMPs). In the CNS, MMPs are synthesized by resident glial cells and affect the integrity of the neuropil extracellular matrix (ECM). To ascertain how MMPs influence HAD pathogenesis, we studied their secretion following MP differentiation, viral infection, and cellular activation. HIV-1-infected and/or immune-activated monocyte-derived macrophages (MDM) and human fetal microglia were examined for production of MMP-1, -2, -3, and -9. MMP expression increased significantly with MP differentiation. Microglia secreted high levels of MMPs de novo that were further elevated following CD40 ligand-mediated cell activation. Surprisingly, HIV-1 infection of MDM led to the down-regulation of MMP-9. In encephalitic brain tissue, MMPs were expressed within perivascular and parenchymal MP, multinucleated giant cells, and microglial nodules. These data suggest that MMP production in MP is dependent on cell type, differentiation, activation, and/or viral infection. Regulation of MMP expression by these factors may contribute to neuropil ECM degradation and leukocyte migration during HAD.

scholarly journals CNNM2-Related Disorders: Phenotype and Its Severity Were Associated With the Mode of Inheritance

2021 ◽  
Vol 9 ◽  
Author(s):  
Han Zhang ◽  
Ye Wu ◽  
Yuwu Jiang
Keyword(s):  
De Novo ◽  
Serum Magnesium ◽  
Brain Magnetic Resonance Imaging ◽  
Functional Studies ◽  
Pathogenic Variants ◽  
Significant Difference ◽  
Domain Variations ◽  
Type 3

CNNM2 (Cystathionine-β-synthase-pair Domain Divalent Metal Cation Transport Mediator 2) pathogenic variants have been reported to cause hypomagnesemia, epilepsy, and intellectual disability/developmental delay (ID/DD). We identified two new cases with CNNM2 novel de novo pathogenic variants, c.814T>C and c.976G>C. They both presented with infantile-onset epilepsy with DD and hypomagnesemia refractory to magnesium supplementation. To date, 21 cases with CNNM2-related disorders have been reported. We combined all 23 cases to analyze the features of CNNM2-related disorders. The phenotypes can be classified into three types: type 1, autosomal dominant (AD) inherited simple hypomagnesemia; type 2, AD inherited hypomagnesemia with epilepsy and ID/DD; and type 3, autosomal recessive (AR) inherited hypomagnesemia with epilepsy and ID/DD. All five type 1 cases had no epilepsy or ID/DD; they all had hypomagnesemia, and three of them presented with symptoms secondary to hypomagnesemia. Fifteen type 2 patients could have ID/DD and seizures, which can be controlled with antiseizure medications (ASMs); their variations clustered in the DUF21 domain of CNNM2. All three type 3 patients had seizures from 1 to 6 days after birth; the seizures were refractory, and 1/3 had status epilepticus; ID/DD in these AR-inherited cases was more severe than that of AD-inherited cases; they all had abnormalities of brain magnetic resonance imaging (MRI). Except for one patient whose serum magnesium was the lower limit of normal, others had definite hypomagnesemia. Hypomagnesemia could be improved after magnesium supplement but could not return to the normal level. Variations in the CBS2 domain may be related to lower serum magnesium. However, there was no significant difference in the level of serum magnesium among the patients with three different types of CNNM2-related disorders. The severity of different phenotypes was therefore not explained by decreased serum magnesium. We expanded the spectrum of CNNM2 variants and classified the phenotypes of CNNM2-related disorders into three types. We found that DUF21 domain variations were most associated with CNNM2-related central nervous system phenotypes, whereas hypomagnesemia was more pronounced in patients with CBS2 domain variations, and AR-inherited CNNM2-related disorders had the most severe phenotype. These results provide important clues for further functional studies of CNNM2 and provide basic foundations for more accurate genetic counseling.

scholarly journals Persistent epigenetic memory impedes rescue of the telomeric phenotype in human ICF iPSCs following DNMT3B correction

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Shir Toubiana ◽  
Miriam Gagliardi ◽  
Mariarosaria Papa ◽  
Roberta Manco ◽  
Maty Tzukerman ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Dna Methyltransferase ◽  
De Novo ◽  
Pharmacological Intervention ◽  
Icf Syndrome ◽  
Genome Wide ◽  
Mammalian Genomes ◽  
Induced Pluripotent ◽  
Methylation Patterns

DNA methyltransferase 3B (DNMT3B) is the major DNMT that methylates mammalian genomes during early development. Mutations in human DNMT3B disrupt genome-wide DNA methylation patterns and result in ICF syndrome type 1 (ICF1). To study whether normal DNA methylation patterns may be restored in ICF1 cells, we corrected DNMT3B mutations in induced pluripotent stem cells from ICF1 patients. Focusing on repetitive regions, we show that in contrast to pericentromeric repeats, which reacquire normal methylation, the majority of subtelomeres acquire only partial DNA methylation and, accordingly, the ICF1 telomeric phenotype persists. Subtelomeres resistant to de novo methylation were characterized by abnormally high H3K4 trimethylation (H3K4me3), and short-term reduction of H3K4me3 by pharmacological intervention partially restored subtelomeric DNA methylation. These findings demonstrate that the abnormal epigenetic landscape established in ICF1 cells restricts the recruitment of DNMT3B, and suggest that rescue of epigenetic diseases with genome-wide disruptions will demand further manipulation beyond mutation correction.

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