Allele-Specific Transcriptional Regulation of Shoot Regeneration in Hybrid Poplar

Plant tissue regeneration is a key process for genetic transformation and genome editing. The exploration of regulatory mechanisms in plant regeneration would improve regeneration efficiency. In comparison to some model plants, the genomic heterozygosity is much higher in forest trees, increasing the complexity of transcriptional regulation. Here, we report the allele-specific transcriptional analysis in hybrid poplar 84K (Populus alba × P. tremula var. glandulosa cv. 84K) during the shoot regeneration process. Firstly, 180 regeneration-related genes (REGs) and 2446 REG-homologous genes (REGHs) were identified in hybrid poplar. The expression patterns of REGs exhibited that about half of them were positively correlated between poplar and Arabidopsis at the locus level. The expression levels of REGHs vary among the gene family at different stages during callus and shoot induction. Among the gene clusters with similar expression patterns, the distribution of gene families in poplar and Arabidopsis also exhibits large variations. At the allele level, most of the allele pairs of REGs were positively correlated in expression. The expression patterns of genes in auxin synthesis, transport, and signaling pathways agree with the general patterns. Due to the presence/absence of variations between two subgenomes, two YUC alleles and two IAA alleles are present only in one subgenome, and the expression patterns of the two alleles are greatly different. Our analysis indicates the conservativeness and diversity of transcriptional regulation during shoot regeneration in poplar and Arabidopsis. The complexity in allele expression contributed by heterozygosity suggests the importance of genotyping in the screening of explants for plant regeneration

Maternal dyslipidemia during pregnancy may increase the risk of preterm birth: A meta-analysis

Epidemiological studies have reported an inconsistent relationship between maternal lipid levels and preterm birth (PTB). We performed this meta-analysis to evaluate the association between maternal dyslipidemia and PTB. Overall, three nested case-control studies and eight cohort studies were eligible. Effect estimates [odds ratio(OR)/relative risk] were pooled using a fixed-effects or a random-effects model. Subgroup and metaregression analyses were conducted to evaluate the sources of heterogeneity. Eleven studies involving 13,025 pregnant women were included. Compared with pregnant women with normal lipid levels, the women with elevated levels of lipids had an increased risk of PTB, and the pooled OR was 1.68 [95% confidence interval (CI): 1.25–2.26)]; meanwhile, women with lower levels of lipids also had a trend of an increased risk of PTB (OR=1.52, 95% CI=0.60–3.82). The pooled ORs for elevated levels of total cholesterol, triglycerides, low density lipoprotein-cholesterol, and lower levels of high density lipoprotein-cholesterol were 1.71 (95% CI: 1.05–2.79), 1.55 (95% CI: 1.13–2.12), 1.19 (95% CI: 0.95–1.48), and 1.33 (95% CI: 1.14–1.56), respectively. The present meta-analysis found that maternal dyslipidemia during pregnancy, either the elevated total cholesterol or triglycerides, was associated with an increased risk of PTB. These findings indicate that a normal level of maternal lipid during pregnancy may reduce the risk of PTB

Autophagy impairment with lysosomal and mitochondrial dysfunction is an important characteristic of oxidative stress-induced senescence

<p>Macroautophagy/autophagy has profound implications for aging. However, the true features of autophagy in the progression of aging remain to be clarified. In the present study, we explored the status of autophagic flux during the development of cell senescence induced by oxidative stress. In this system, although autophagic structures increased, the degradation of SQSTM1/p62 protein, the yellow puncta of mRFP-GFP-LC3 fluorescence and the activity of lysosomal proteolytic enzymes all decreased in senescent cells, indicating impaired autophagic flux with lysosomal dysfunction. The influence of autophagy activity on senescence development was confirmed by both positive and negative autophagy modulators; and MTOR-dependent autophagy activators, rapamycin and PP242, efficiently suppressed cellular senescence through a mechanism relevant to restoring autophagic flux. By time-phased treatment of cells with the antioxidant N-acetylcysteine (NAC), the mitochondria uncoupler carbonyl cyanide m-chlorophenyl hydrazone (CCCP) and ambroxol, a reagent with the effect of enhancing lysosomal enzyme maturation, we found that mitochondrial dysfunction plays an initiating role, while lysosomal dysfunction is more directly responsible for autophagy impairment and senescence. Interestingly, the effect of rapamycin on autophagy flux is linked to its role in functional revitalization of both mitochondrial and lysosomal functions. Together, this study demonstrates that autophagy impairment is crucial for oxidative stress-induced cell senescence, thus restoring autophagy activity could be a promising way to retard senescence.</p

Active DNA unwinding and transport by a membrane-adapted helicase nanopore.

Nanoscale transport through nanopores and live-cell membranes plays a vital role in both key biological processes as well as biosensing and DNA sequencing. Active translocation of DNA through these nanopores usually needs enzyme assistance. Here we present a nanopore derived from truncated helicase E1 of bovine papillomavirus (BPV) with a lumen diameter of c.a. 1.3 nm. Cryogenic&nbsp;electron microscopy (cryo-EM) imaging and single channel recording confirm its insertion into planar lipid bilayer (BLM). The helicase nanopore in BLM allows the passive single-stranded DNA (ssDNA) transport and retains the helicase activity in vitro. Furthermore, we incorporate this helicase nanopore into the live cell membrane of HEK293T cells, and monitor the ssDNA delivery into the cell real-time at single molecule level. This type of nanopore is expected to provide an interesting tool to study the biophysics of biomotors in vitro, with potential applications in biosensing, drug delivery and real-time single cell analysis