Biology subjects

An, W.

Publications and source records attributed to An, W..

3 recordsLinked to original sources

bioRxiv2018

Virus infection might cause cells producing black swimming dots

Black swimming dots (BSDs) are nanoscale dot-like contaminants in the dishes of cultured cells. Until now, the identity of BSDs has not yet been determined. In our recent study, we proposed that BSDs per se are nonliving inorganic nanoparticles yet should derive from the cells infected with an unidentified airborne pathogen. We showed the pathogen possessed the characteristics including airborne transmitted, cell-dependent, insensitive to antibiotics, filterable through 0.1 m membrane. These properties prompt us to speculate that the pathogen of BSDs might be one kind of unidentified virus-like organism. However, the imperfection is that we have not isolated this putative pathogen from BSD+ samples [1]. Here, we report a further investigation of finding the virus-like pathogen in the serum and tissue extracts from BSD+ mice. Most importantly, this virus-like pathogen can be reisolated from the BSD+ extracts-inoculated, diseased BSD- cells.\n\nTo de ...

cell biology↗

bioRxiv2018

Black swimming dots in cell culture: the identity, detection method and judging criteria

Black swimming dots (BSDs) -- the biological UFO in cell culture -- have perplexed biologists for decades. BSDs are extremely tiny dots found in dishes of cultured cells. It is still controversial on their origin and identity. BSDs are very hard to be removed and bring adverse impact to cell experiments (Supplementary Table 1). Here we wish to answer three urgent questions about BSDs. First, is the identity of BSDs nonliving matter or living organism? Second, is there any reliable method to tell whether the donor cattle for FBS production or the animals for primary cells isolation carry BSDs? Third, what are the judging criteria for BSDs when \"tiny black dots\" were observed? In 2015, we happened to observe BSDs in the perivitelline space of mouse oocytes and embryos; and the cells derived from these mice exhibited typical properties of BSDs infected cells (described in Supplementary Information). With these BSDs infected (BSD+) mice, we demonstrate that BSDs per se are ...

cell biology↗

bioRxiv2018

Heterogeneity of transposon expression and activation of the repressive network in human fetal germ cells

Epigenetic resetting in germ cells during development leads to the de-repression of transposable elements (TEs). piRNAs protect fetal germ cells from potentially harmful TEs by targeted destruction of mRNA and deposition of repressive epigenetic marks. Here we provide the first evidence for an active piRNA pathway and TE repression in germ cells of human fetal testis. We identify pre-pachytene piRNAs with features of secondary amplification that map most abundantly to L1 family TEs. We find that L1-ORF1p expression is heterogeneous in fetal germ cells, peaks at mid-gestation and declines concomitantly with increasing levels of piRNAs and H3K9me3, as well as nuclear localization of HIWI2. Surprisingly, following this decline, the same cells with accumulation of L1-ORF1p display highest levels of HIWI2 and H3K9me3, whereas L1-ORF1p low cells are also low in HIWI2 and H3K9me3. Conversely, earlier in development, the germ cells lacking L1-ORF1p express high levels of the chaperone HSP90a. We propose that a subset of HSP90a-armed germ cells resists L1 expression, whereas only those vulnerable L1-expressing germ cells activate the PIWI-piRNA repression pathway which leads to epigenetic silencing of L1 via H3K9me3.

developmental biology↗