Florigen goes molecular: Seventy years of the hormonal theory of flowering regulation

As early as in 1936, the comprehensive studies of flowering led M.Kh. Chailakhyan to the concept of florigen, a hormonal floral stimulus, and let him establish several characteristics of this stimulus. These studies set up for many years the main avenues for research into the processes that control plant flowering, and the notion of florigen became universally accepted by scientists worldwide. The present-day evidence of genetic control of plant flowering supports the idea that florigen participates in floral signal transduction. The recent study of arabidopsis plants led the authors to conclusion that the immediate products of the gene FLOWERING LOCUS I, its mRNA and/or protein, move from an induced leaf into the shoot apex and evoke flowering therein.     

Overexpression of gene PPZ1 in the yeast Saccharomyces cerevisiae affects the efficiency of nonsense suppression

The phenomenon of nonsense suppression, which leads to the stop codons reading-through, may be related to disturbances in the operation of various components of the translation apparatus and the proteins interacting with them. The phosphatase Ppzlp is one of the factors affecting the nonsense suppression efficiency in Saccharomyces yeast. In this work, the impact of the overexpression of gene PPZ1 and its mutant allele PPZ1-R451L on the phenotypic expression of various mutant alleles of genes SUP35 and SUP45 or the yeast prion [PSI ⁺] was analyzed. On the basis of the data obtained, a suggestion about the possible role of proteins Sup35p and Sup45p in the processes mediating the influence of gene PPZ1 overexpression on the efficiency of nonsense suppression is made.     

Cellular and regional localization of the neurospecific antigen 10-40-4 in the human brain

Cellular and regional localization of neurospecific protein 10-40-4 in human brain was studied by immunofluorescent staining and immunoenzymatic assay. Intense fluorescence of perikaryons of the medulla oblongata, thalamus and pons neurons was demonstrated. The same structures showed the maximal concentration of the protein (15-18% of water-soluble proteins). In the cortex of the hemispheres, in the cerebellum and hypothalamus the fluorescence intensity was not different from the background level. The concentration of the protein in these structures was minimal (1-4% of water-soluble proteins).     

CARD15 and TLR4 polymorphisms in atopic bronchial asthma

In order to investigate whether single nucleotide polymorphisms G(+2722)C and 3020insC of CARD15 and Asp299Gly of TLR4 contribute to atopic bronchial asthma, we performed a comparative analysis of allele and genotype frequencies of these polymorphisms in Russian patients from Moscow. DNA specimens obtained from 283 patients with atopic bronchial asthma and 227 healthy donors were genotyped. Neither G(+2722)C or 3020insC in CARD15 nor Asp299Gly in TLR4 were associated with asthma; CARD15 polymorphisms were not also associated with asthma severity. A haplotype frequency analysis of CARD15 polymorphisms did not detect significant differences between the groups studied. However, a strong association was found between Asp299Gly and asthma course: the Asp allele was associated with mild disease, while the minor Gly allele was associated with moderate/severe asthma (OR = 0.47, 95% CI [0.24–0.93] and OR = 2.12, 95% CI [1.08–4.18], respectively).     

Synaptodendritic recovery following HIV Tat exposure: Neurorestoration by phytoestrogens

HIV‐1 infects the brain and, despite antiretroviral therapy, many infected individuals suffer from HIV‐1‐associated neurocognitive disorders (HAND). HAND is associated with dendritic simplification and synaptic loss. Prevention of synaptodendritic damage may ameliorate or forestall neurocognitive decline in latent HIV‐1 infections. The HIV‐1 transactivating protein (Tat) is produced during viral latency in the brain and may cause synaptodendritic damage. This study examined the integrity of the dendritic network after exposure to HIV‐1 Tat by labeling filamentous actin (F‐actin)‐rich structures (puncta) in primary neuronal cultures. After 24 h of treatment, HIV‐1 Tat was associated with the dendritic arbor and produced a significant reduction of F‐actin‐labeled dendritic puncta as well as loss of dendrites. Pre‐treatment with either of two plant‐derived phytoestrogen compounds (daidzein and liquiritigenin), significantly reduced synaptodendritic damage following HIV‐1 Tat treatment. In addition, 6 days after HIV‐1 Tat treatment, treatment with either daidzein, or liquiritigenin enhanced recovery, via the estrogen receptor, from HIV‐1 Tat‐induced synaptodendritic damage. These results suggest that either liquiritigenin or daidzein may not only attenuate acute synaptodendritic injury in HIV‐1 but may also promote recovery from synaptodendritic damage.

     

Glutamine Synthetase-Induced Enhancement of β-Amyloid Peptide Aβ(1–40) Neurotoxicity Accompanied by Abrogation of Fibril Formation and Aβ Fragmentation

Abstract: β-Amyloid peptide (Aβ) is the main constituent in both senile plaques and diffuse deposits in Alzheimer's diseased brains. It was previously shown that synthetic Aβs were able to form free radical species in aqueous solution and cause both oxidative damage to cell proteins and inactivation of key metabolic enzymes. We also previously demonstrated that an interaction of Aβ(1–40) with the oxidatively sensitive enzyme glutamine synthetase (GS) resulted in both inactivation of GS and an increase of Aβ toxicity to hippocampal cell cultures. In the present study the enhancement of Aβ toxicity during interaction with GS was found to be accompanied by abrogation of fibril formation and partial fragmentation of Aβ(1–40). HPLC elution profiles demonstrated the production of several peptide fragments. Analysis of the amino acid sequence of the major fragments identified them as the first 15 and the last six amino acids of Aβ(1–40). The fragmentation of Aβ was inhibited by immunoprecipitation of GS.     

Effect of Ca2+ on the motility of myosin head in the F-actin-HMM complex

Using polarization microfluorimetry, the effect of Ca2+ on the mode of interaction between heavy meromyosin labeled with 1.5-IAEDANS and F-actin was studied. The results obtained suggest that both the orientation and motility of myosin heads in the F-actin-heavy meromyosin complex depend on Ca2+ concentration. The experimental results are suggestive of the existence of a myosin-coupled regulatory system in skeletal muscles.