NYD-SP16, a novel gene associated with spermatogenesis of human testis

By hybridizing human adult testis cDNA microarrays with human adult and embryo testis cDNA probes, a novel human testis gene NYD-SP16 was identified. NYD-SP16 expression was 6.44-fold higher in adult testis than in fetal testis. NYD-SP16 contains 1595 base pairs (bp) and a 762-bp open reading frame encoding a 254-amino acid protein with 73% amino acid sequence identity with the mouse testis homologous protein. The NYD-SP16 gene was localized to human chromosome 5q14. The deduced structure of the NYD-SP16 protein contains one transmembrane domain, which was confirmed by GFP/NYD-SP16 fusion protein expression in the cytomembrane of the transfected human choriocarcinoma JAR cells, suggesting that it is a transmembrane protein. Multiple tissue distribution indicated that NYD-SP16 mRNA is highly expressed in the testes and pancreas, with little or no expression elsewhere. Further analysis of abnormal expression in infertile male patients revealed complete absence of NYD-SP16 in the testes of patients with Sertoli-cell-only syndrome and variable expression in patients with spermatogenic arrest. Homologous gene expression in mouse testis was confirmed in spermatogenic cells by in situ hybridization. The results of cDNA microarray, in situ hybridization, and semiquantitative polymerase chain reaction in mouse testis of different stages indicated that NYD-SP16 expression is developmentally regulated. These results suggest that the putative NYD-SP16 protein may play an important role in testicular development/spermatogenesis and may be an important factor in male infertility.     

Oxidative damage to 5-methylcytosine in DNA.

Exposure of pyrimidines of DNA to ionizing radiation under aerobic conditions or oxidizing agents results in attack on the 5,6 double bond of the pyrimidine ring or on the exocyclic 5-methyl group. The primary product of oxidation of the 5,6 double bond of thymine is thymine glycol, while oxidation of the 5-methyl group yields 5-hydroxymethyluracil. Oxidation of the 5,6 double bond of cytosine yields cytosine glycol, which decomposes to 5-hydroxycytosine, 5-hydroxyuracil and uracil glycol, all of which are repaired in DNA by Escherichia coli endonuclease III. We now describe the products of oxidation of 5-methylcytosine in DNA. Poly(dG-[3H]dmC) was gamma-irradiated or oxidized with hydrogen peroxide in the presence of Fe3+ and ascorbic acid. The oxidized co-polymer was incubated with endonuclease III or 5-hydroxymethyluracil-DNA glycosylase, to determine whether repairable products were formed, or digested to 2'-deoxyribonucleosides, to determine the total complement of oxidative products. Oxidative attack on 5-methylcytosine resulted primarily in formation of thymine glycol. The radiogenic yield of thymine glycol in poly(dG-dmC) was the same as that in poly(dA-dT), demonstrating that 5-methylcytosine residues in DNA were equally susceptible to radiation-induced oxidation as were thymine residues.     

Plant functional diversity enhances associations of soil fungal diversity with vegetation and soil in the restoration of semiarid sandy grassland

The trait‐based approach shows that plant functional diversity strongly affects ecosystem properties. However, few empirical studies show the relationship between soil fungal diversity and plant functional diversity in natural ecosystems. We investigated soil fungal diversity along a restoration gradient of sandy grassland (mobile dune, semifixed dune, fixed dune, and grassland) in Horqin Sand Land, northern China, using the denaturing gradient gel electrophoresis of 18S rRNA and gene sequencing. We also examined associations of soil fungal diversity with plant functional diversity reflected by the dominant species' traits in community (community‐weighted mean, CWM) and the dispersion of functional trait values (FD_is). We further used the structure equation model (SEM) to evaluate how plant richness, biomass, functional diversity, and soil properties affect soil fungal diversity in sandy grassland restoration. Soil fungal richness in mobile dune and semifixed dune was markedly lower than those of fixed dune and grassland (P < 0.05). Soil fungal richness was positively associated with plant richness, biomass, CWM plant height, and soil gradient aggregated from the principal component analysis, but SEM results showed that plant richness and CWM plant height determined by soil properties were the main factors exerting direct effects. Soil gradient increased fungal richness through indirect effect on vegetation rather than direct effect. The negative indirect effect of FDis on soil fungal richness was through its effect on plant biomass. Our final SEM model based on plant functional diversity explained nearly 70% variances of soil fungal richness. Strong association of soil fungal richness with the dominant species in the community supported the mass ratio hypothesis. Our results clearly highlight the role of plant functional diversity in enhancing associations of soil fungal diversity with community structure and soil properties in sandy grassland ecosystems.     

Double the Capacity of Manganese Spinel for Lithium‐Ion Storage by Suppression of Cooperative Jahn–Teller Distortion

The relatively low capacity and capacity fade of spinel LiMn₂O₄ (LMO) limit its application as a cathode material for lithium‐ion batteries. Extending the potential window of LMO below 3 V to access double capacity would be fantastic but hard to be realized, as it will lead to fast capacity loss due to the serious Jahn–Teller distortion. Here using experiments combined with extensive ab initio calculations, it is proved that there is a cooperative effect among individual Jahn–Teller distortions of Mn³⁺O₆ octahedrons in LMO, named as cooperative Jahn–Teller distortion (CJTD) in the text, which is the difficulty to access the capacity beyond one lithium intercalation. It is further proposed that the cationic disordering (excess Li at Mn sites and Li/Mn exchange) can intrinsically suppress the CJTD of Mn³⁺O₆ octahedrons. The cationic disordering can break the symmetry of Mn³⁺ arrangements to disrupt the correlation of distortions arising from individual JT centers and prevent the Mn³⁺? O bonds distorting along one direction. Interestingly, with the suppressed CJTD, the original octahedral vacancies in spinel LMO are activated and can serve as extra Li‐ion storage sites to access the double capacity with good reversible cycling stability in microsized LMO.     

Correction to: Development of a Novel Reverse Transcription Loop-Mediated Isothermal Amplification Method for Rapid Detection of SARS-CoV-2

Virologica Sinica - The corrected legend is given below.     

DNA framework-engineered electrochemical biosensors

Self-assembled DNA nanostructures have shown remarkable potential in the engineering of biosensing interfaces, which can improve the performance of various biosensors. In particular, by exploiting the structural rigidity and programmability of the framework nucleic acids with high precision, molecular recognition on the electrochemical biosensing interface has been significantly enhanced, leading to the development of highly sensitive and specific biosensors for nucleic acids, small molecules,proteins, and cells. In this review, we summarize recent advances in DNA framework-engineered biosensing interfaces and the application of corresponding electrochemical biosensors.     

Tau inhibits PKA by nuclear proteasome‐dependent PKAR2α elevation with suppressed CREB/GluA1 phosphorylation

Intraneuronal accumulation of wild‐type tau plays a key role in Alzheimer's disease, while the mechanisms underlying tauopathy and memory impairment remain unclear. Here, we report that overexpressing full‐length wild‐type human tau (hTau) in mouse hippocampus induces learning and memory deficits with remarkably reduced levels of multiple synapse‐ and memory‐associated proteins. Overexpressing hTau inhibits the activity of protein kinase A (PKA) and decreases the phosphorylation level of cAMP‐response element binding protein (CREB), GluA1, and TrkB with reduced BDNF mRNA and protein levels both in vitro and in vivo. Simultaneously, overexpressing hTau increased PKAR2α (an inhibitory subunit of PKA) in nuclear fraction and inactivated proteasome activity. With an increased association of PKAR2α with PA28γ (a nuclear proteasome activator), the formation of PA28γ‐20S proteasome complex remarkably decreased in the nuclear fraction, followed by a reduced interaction of PKAR2α with 20S proteasome. Both downregulating PKAR2α by shRNA and upregulating proteasome by expressing PA28γ rescued hTau‐induced PKA inhibition and CREB dephosphorylation, and upregulating PKA improved hTau‐induced cognitive deficits in mice. Together, these data reveal that intracellular tau accumulation induces synapse and memory impairments by inhibiting PKA/CREB/BDNF/TrkB and PKA/GluA1 signaling, and deficit of PA28γ‐20S proteasome complex formation contributes to PKAR2α elevation and PKA inhibition.