Publications by authors named "K V Trofimov"
In the dynamic environment of plants, the interplay between light-dependent growth and iron nutrition is a recurring challenge. Plants respond to low iron levels by adjusting growth and physiology through enhanced iron acquisition from the rhizosphere and internal iron pool reallocation. Iron deficiency response assays and gene co-expression networks aid in documenting physiological reactions and unraveling gene regulatory cascades, offering insight into the interplay between hormonal and external signaling pathways.
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- Iron (Fe) is an essential micronutrient for plants, and its uptake is regulated to prevent toxicity, with the POPEYE (PYE) transcription factor playing a key role in this process.
- In PYE's absence, plants exhibit altered Fe distribution leading to leaf chlorosis, and levels of certain genes (NAS4, FRO3, ZIF1) increase.
- The study identifies a protein called OLIVIA (OLV), which interacts with PYE, and suggests that OLV may play a role in linking iron homeostasis to leaf growth regulation.
The functional importance of nuclear protein condensation remains often unclear. The bHLH FER-like iron deficiency-induced transcription factor (FIT) controls iron acquisition and growth in plants. Previously described C-terminal serine residues allow FIT to interact and form active transcription factor complexes with subgroup Ib bHLH factors such as bHLH039.
View Article and Find Full Text PDFAtherosclerosis is associated with a chronic local inflammatory process in the arterial wall. Our previous studies have demonstrated the altered proinflammatory activity of circulating monocytes in patients with atherosclerosis. Moreover, atherosclerosis progression and monocyte proinflammatory activity were associated with mitochondrial DNA (mtDNA) mutations in circulating monocytes.
View Article and Find Full Text PDFRegulation of iron (Fe) acquisition and homeostasis is critical for plant survival. In Arabidopsis, Fe deficiency-induced bHLH039 forms a complex with the master regulator FIT and activates it to upregulate Fe acquisition genes. FIT is partitioned between cytoplasm and nucleus, whereby active FIT accumulates more in the nucleus than inactive FIT.
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