Length-to-weight and length-to-length ratios of six cavefish species from the Pearl River Basin,South China

Length-to-weight and length-to-length ratios were estimated for six cavefishes including Yunnanilus longibarbatus, Yunnanilus bailianensis, Yunnanilus jinxiensis, Oreonectes polystigmus, Paranemachilus pingguoensis, and Paranemachilus genilepis from the upper reaches of the Pearl River, Guangxi Province, China (between 106.26E, 23.14N and 111.42E, 24.85N). The fish were captured between May and October in 2018 and 2019 using trap nets (mesh size 7 mm) set in front of selected caves at 6:30–7:30 p.m. and were hauled out at 6:30–7:30 a.m. the next day. After removal, the fish were measured and weighed immediately to the nearest 0.1 cm and 0.1 g, respectively. The regression parameter r² was between .95 and .98. The total length-to-standard length ratios were also calculated with r² ≥ .98. This study should provide a useful reference for biological studies and biodiversity conservation of cavefish.     

Genetic diversity of mitochondrial D-LOOP sequences in the spotted scat (Scatophagus argus) from different geographical populations along the northern coast of the South China Sea

The genetic diversity of 289 spotted scat (Scatophagus argus) from seven populations along the northern coast of the South China Sea was studied by analyzing the full-length sequences of the mitochondrial control region (D-LOOP). The S. argus D-LOOP sequence was 1,004–1,010 bp long and contained 156 variant sites. The seven studied S. argus populations had a high degree of genetic diversity (haplotype diversity [Hd] = 0.99135; nucleotide diversity (π) = 0.01313). There was no obvious genetic differentiation among the seven geographical populations and gene exchange was frequent (Fst = −0.01867–0.01117, p > .05). Four distinct mitochondrial lineages were identified in the phylogenetic tree and the haplotype network. The between-lineage Fst was 0.71690–0.84940 (p < .001), but these lineages showed no obvious phylogeographic pattern. Based on D-LOOP mutation rates, we estimated that the four lineages diverged approximately 513,800–93,600 years ago, during the Eocene ice age, at which time falling sea levels may have led to population segregation. We estimated that S. argus population expansion occurred approximately 2.29–0.68 million years ago, during the late Pleistocene. During this period, sea levels rose again, allowing previously separated lineages to come into sympatry, which eventually gave rise to a highly genetically diverse population without pyhlogeographic structure. Here, we characterized the genetic structure and differentiation of seven S. argus populations from the northern coast of the South China Sea. Our results suggested that the seven S. argus populations from the northern coast of the South China Sea have a relatively low level of genetic variation and can be considered a single unit for the purposes of fishery development, utilization, and management.     

miR-194-5p negatively regulates the proliferation and differentiation of rabbit skeletal muscle satellite cells

Molecular and Cellular Biochemistry - Skeletal muscle satellite cells (SMSCs), also known as a multipotential stem cell population, play a crucial role during muscle growth and regeneration. In...     

Studies on the effects of bone marrow stem cells on mitochondrial function and the alleviation of ARDS

Molecular and Cellular Biochemistry - Mesenchymal stem cells (MSCs) can alleviate acute respiratory distress syndrome (ARDS), but the mechanisms involved are unclear, especially about their...     

The involvement of bioactive factors in the self-renewal and stemness maintenance of spermatogonial stem cells

Molecular and Cellular Biochemistry - Spermatogenesis is usually accompanied throughout mammalian lifetime, transmitting genetic information to the next generation, which is mainly dependent on the...     

Uniparental isodisomy of chromosome 2 causing MRPL44-related multisystem mitochondrial disease

Mutations in nuclear-encoded protein subunits of the mitochondrial ribosome are an increasingly recognised cause of oxidative phosphorylation system (OXPHOS) disorders. Among them, mutations in the MRPL44 gene, encoding a structural protein of the large subunit of the mitochondrial ribosome, have been identified in four patients with OXPHOS defects and early-onset hypertrophic cardiomyopathy with or without additional clinical features. A 23-year-old individual with cardiac and skeletal myopathy, neurological involvement, and combined deficiency of OXPHOS complexes in skeletal muscle was clinically and genetically investigated. Analysis of whole-exome sequencing data revealed a homozygous mutation in MRPL44 (c.467 T?>?G), which was not present in the biological father, and a region of homozygosity involving most of chromosome 2, raising the possibility of uniparental disomy. Short-tandem repeat and genome-wide SNP microarray analyses of the family trio confirmed complete maternal uniparental isodisomy of chromosome 2. Mitochondrial ribosome assembly and mitochondrial translation were assessed in patient derived-fibroblasts. These studies confirmed that c.467 T?>?G affects the stability or assembly of the large subunit of the mitochondrial ribosome, leading to impaired mitochondrial protein synthesis and decreased levels of multiple OXPHOS components. This study provides evidence of complete maternal uniparental isodisomy of chromosome 2 in a patient with MRPL44-related disease, and confirms that MRLP44 mutations cause a mitochondrial translation defect that may present as a multisystem disorder with neurological involvement.

     

Post-translational modification of RNA m6A demethylase ALKBH5 regulates ROS-induced DNA damage response

Faithful genome integrity maintenance plays an essential role in cell survival. Here, we identify the RNA demethylase ALKBH5 as a key regulator that protects cells from DNA damage and apoptosis during reactive oxygen species (ROS)-induced stress. We find that ROS significantly induces global mRNA N⁶-methyladenosine (m⁶A) levels by modulating ALKBH5 post-translational modifications (PTMs), leading to the rapid and efficient induction of thousands of genes involved in a variety of biological processes including DNA damage repair. Mechanistically, ROS promotes ALKBH5 SUMOylation through activating ERK/JNK signaling, leading to inhibition of ALKBH5 m⁶A demethylase activity by blocking substrate accessibility. Moreover, ERK/JNK/ALKBH5-PTMs/m⁶A axis is activated by ROS in hematopoietic stem/progenitor cells (HSPCs) in vivo in mice, suggesting a physiological role of this molecular pathway in the maintenance of genome stability in HSPCs. Together, our study uncovers a molecular mechanism involving ALKBH5 PTMs and increased mRNA m⁶A levels that protect genomic integrity of cells in response to ROS.     

Hyaluronan synthase 2 (HAS2) regulates cell phenotype and invadopodia formation in luminal-like breast cancer cells

Molecular and Cellular Biochemistry - Although luminal breast cancer cells are typically highly cohesive epithelial cells and have low invasive ability, many eventually develop metastasis. Until...