Antibiotic-resistant P. acnes is prevalent in Hong Kong. Dermatologists should be more vigilant in prescribing antibiotics for acne patients.

Small nucleolar RNAs (snoRNAs) and Cajal body-specific RNAs (scaRNAs) are named for their subcellular localization within nucleoli and Cajal bodies (conserved subnuclear organelles present in the nucleoplasm), respectively. They have been found to play important roles in rRNA, tRNA, snRNAs, and even mRNA modification and processing. All snoRNAs fall in two categories, box C/D snoRNAs and box H/ACA snoRNAs, according to their distinct sequence and secondary structure features. Box C/D snoRNAs and box H/ACA snoRNAs mainly function in guiding 2′-O-ribose methylation and pseudouridilation, respectively. ScaRNAs possess both box C/D snoRNA and box H/ACA snoRNA sequence motif features, but guide snRNA modifications that are transcribed by RNA polymerase II. Here we present a Web-based sno/scaRNA database, called sno/scaRNAbase, to facilitate the sno/scaRNA research in terms of providing a more comprehensive knowledge base. Covering 1979 records derived from 85 organisms for the first time, sno/scaRNAbase is not only dedicated to filling gaps between existing organism-specific sno/scaRNA databases that are focused on different sno/scaRNA aspects, but also provides sno/scaRNA scientists with an opportunity to adopt a unified nomenclature for sno/scaRNAs. Derived from a systematic literature curation and annotation effort, the sno/scaRNAbase provides an easy-to-use gateway to important sno/scaRNA features such as sequence motifs, possible functions, homologues, secondary structures, genomics organization, sno/scaRNA gene's chromosome location, and more. Approximate searches, in addition to accurate and straightforward searches, make the database search more flexible. A BLAST search engine is implemented to enable blast of query sequences against all sno/scaRNAbase sequences. Thus our sno/scaRNAbase serves as a more uniform and friendly platform for sno/scaRNA research. The database is free available at .

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Abstract. Although many studies have been conducted on the interspecific competition between new arrivals and native plants, few of them have demonstrated how these processes interact with non-resource factors to determine vegetation pattern. This study investigated how salt stress mediates competition between native Phragmites australis and invasive Spartina alterniflora and thus changes plant communities in Dongtan, a Chinese coast salt marsh. The experiments revealed that the growth and reproduction of the native species declined with increasing salinity but that the invasive species performed well in the salinity range of 0-20%, illustrating why the invader could proliferate in the high salinity mudflats in Dongtan. Moreover, the native had a high growth rate and therefore exhibited a competitive dominance over the invader at low salinity of ca. 7%. Thus, the invader could not displace the native, and the native communities were stable in the low salinity zones. In contrast, the growth rate of the invader became higher when salinity increased; correspondingly, it gained the competitive dominance at high salinity of ca. 11%. As a result, the invader colonising the native communities in high salinity zones performed better and could displace the natives over time. Consequently, after invasive S. alterniflora colonisation, the vegetation pattern of Dongtan marsh gradually changed from ''mudflat-sedge-P. australis'' to ''mudflat-S. alterniflora'' and ''mudflat-S. alterniflora and natives'' along the elevation gradients. The findings of the case study demonstrated that if a new arrival has a wide tolerance range to major non-resource stress in an ecosystem, it can not only displace natives by interspecific competition in high stress zones but can also spread into the zones without natives; on the other hand, natives with a narrow ecological amplitude in relation to the non-resource stress can only persist in low stress zones. Therefore, the distribution area of new arrivals increases as the distribution area of natives decreases. Because some non-resource stresses have substantial positive effects on native community invasibility, the practices that change the level of non-resource stress and create favorable conditions for invasive species should be stopped.

Next-generation sequencing of the exome and genome of prostate cancers has identified numerous genetic alternations. SPOP (Speckle-type POZ Protein) was one of the most frequently mutated genes in primary prostate cancer, suggesting SPOP is a potential driver of prostate cancer development and progression. However, how SPOP mutations contribute to prostate cancer pathogenesis remains poorly understood. SPOP acts as an adaptor protein of the CUL3-RBX1 E3 ubiquitin ligase complex that generally recruits substrates for ubiquitination and subsequent degradation. ER-localized isoform of the formin protein inverted formin 2 (INF2) mediates actin polymerization at ER-mitochondria intersections and facilitates DRP1 recruitment to mitochondria, which is a critical step in mitochondrial fission. Here, we revealed that SPOP recognizes a Ser/Thr (S/T)-rich motif in the C-terminal region of INF2 and triggers atypical polyubiquitination of INF2. These ubiquitination modifications do not lead to INF2 instability, but rather reduces INF2 localization in ER and mitochondrially associated DRP1 puncta formation, therefore abrogates its ability to facilitate mitochondrial fission. INF2 mutant escaping from SPOP-mediated ubiquitination is more potent in prompting mitochondrial fission. Moreover, prostate cancer-associated SPOP mutants increase INF2 localization in ER and promote mitochondrial fission, probably through a dominant-negative effect to inhibit endogenous SPOP. Moreover, INF2 is important for SPOP inactivation-induced prostate cancer cell migration and invasion. These findings reveal novel molecular events underlying the regulation of INF2 function and localization, and provided insights in understanding the relationship between SPOP mutations and dysregulation of mitochondrial dynamics in prostate cancer.