In leguminous plants, nitrogenase that catalyzes anaerobic symbiotic nitrogen fixation is protected by the sequestration of O2 by Leghemoglobin (LegH). The modulation of the oxygen binding capacity of Hemoglobin (Hb) by different post-translational modifications is well studied; whereas similar studies on LegH's O2 binding are not yet benchmarked. Our results show that in vitro serine phosphorylation of recombinant LegH from Lotus japonicus, a model legume, by a homologous kinase caused a reduction in its oxygen consumption as determined by Clark type electrode. Although mass spectrometry revealed a few phosphorylated serine residues in the LegH, molecular modeling study showed that particularly S45 is the most critical one, along with S55, however the latter with lesser impact on its molecular environment responsible for oxygen consumption. Separate S45D and S55D mutants of recombinant LegH also corroborated the results obtained from molecular modeling study. Thus, this work lays groundwork for further investigation of structural and functional role of serine phosphorylation as one of the mechanisms by which oxygen consumption by LegH may possibly be regulated during nodulation.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10930-015-9608-zDOI Listing

Publication Analysis

Top Keywords

oxygen consumption
12
molecular environment
8
oxygen binding
8
serine phosphorylation
8
recombinant legh
8
molecular modeling
8
modeling study
8
oxygen
5
legh
5
phosphorylation leghemoglobin
4

Similar Publications

Methodological developments in biomedical research are currently moving towards single-cell approaches. This allows for a much better spatial and functional characterization of, for example, the deterioration of cells within a tissue in response to noxae. However, subcellular resolution is also essential to elucidate whether observed impairments are driven by an explicit organelle.

View Article and Find Full Text PDF

Mitochondrial endonuclease G (EndoG) contributes to chromosomal degradation when it is released from mitochondria during apoptosis. It is presumed to also have a mitochondrial function because EndoG deficiency causes mitochondrial dysfunction. However, the mechanism by which EndoG regulates mitochondrial function is not known.

View Article and Find Full Text PDF

Background: Mitochondrial bioenergetics are essential for cellular function, specifically the intricacies of the electron transport chain (ETC), with Complex IV playing a crucial role in unraveling the mechanisms governing energy production. Mathematical models offer a valuable approach to simulate these complex processes, providing insights into normal mitochondrial function and aberrations associated with various diseases, including neurodegenerative disorders. Our research focuses on introducing and refining a mathematical model, emphasizing Complex IV in the ETC, with objectives including incorporating mitochondrial activity modulation using inhibiting and uncoupling reagents, akin to oxygen consumption experiments.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

University of Miami, Coral Gables, FL, USA.

Background: Cerebral blood flow is decreased in mouse models and patients of Alzheimer's disease (AD). We identified that about 2% of cortical capillaries in the APP/PS1 mouse model of AD had stalled blood flow due to neutrophils obstructing capillaries and contributing to vascular inflammation. Neutrophils are more reactive in AD.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Department of Neurology, Mayo Clinic, Rochester, MN, USA.

Background: While disease-modifying treatments that reduce Aβ have been recently approved by the FDA, the identification of novel therapeutic targets and strategies that target underlying mechanisms to delay the AD development are still needed. Abnormal brain energy homeostasis and mitochondria dysfunction are observed early in AD. Therefore, the development of treatments to restore these defects could be beneficial.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!