Autophagy is a fundamental process responsible for degradation and recycling of intracellular contents. In the budding yeast, non-selective macroautophagy and microautophagy of the endoplasmic reticulum (ER) are caused by ER stress, the circumstance where aberrant proteins accumulate in the ER. The more recent study showed that protein aggregation in the ER initiates ER-selective macroautophagy, referred to as ER-phagy; however, the mechanisms by which ER stress induces ER-phagy have not been fully elucidated. Here, we show that the expression levels of ATG39, encoding an autophagy receptor specific for ER-phagy, are significantly increased under ER-stressed conditions. ATG39 upregulation in ER stress response is mediated by activation of its promoter, which is positively regulated by Snf1 AMP-activated protein kinase (AMPK) and negatively by Mig1 and Mig2 transcriptional repressors. In response to ER stress, Snf1 promotes nuclear export of Mig1 and Mig2. Our results suggest that during ER stress response, Snf1 mediates activation of the ATG39 promoter and consequently facilitates ER-phagy by negatively regulating Mig1 and Mig2.

Background The rapid introduction of teleworking due to the coronavirus disease 2019 pandemic has led to concerns about increases in cyberbullying (CB) worldwide. However, little is known about workplace CB in non-Western countries. The first objective was to clarify the prevalence and characteristics regarding workplace CB victimization in Japan. The second objective was to demonstrate the psychological outcomes of CB victimization in combination with traditional bullying (TB). Methods We conducted an anonymous, cross-sectional, Internet-based survey targeting regular employees in Japan (N = 1200) in January 2021. We investigated CB victimization using the Inventory of Cyberbullying Acts at Work and TB victimization by using the Short Negative Act Questionnaire. Possible explanatory factors for TB/CB victimization were sociodemographic variables, personality trait, chronic occupational stress, organizational climate, and gratitude at work. We also measured psychological distress, insomnia, and loneliness to assess adverse effects of workplace bullying. Two-step cluster analysis was used in determining the patterns combined with TB and CB victimization. Hierarchical binomial logistic regression analysis was used. Results In total, 8.0% of employees reported experiencing CB on a weekly basis. CB victimization was associated with younger age, managerial position, higher qualitative workload, and active information dissemination via the Internet, and frequency of teleworking. Three clusters based on TB and CB victimization patterns were identified: those who belong to the first cluster suffered neither from TB and CB (81.0%), the second cluster suffered only from TB (14.3%), and the third cluster suffered from both TB and CB (4.8%). The third cluster exhibited higher odds ratios (ORs) and 95% confidence intervals (CIs) for psychological distress (OR = 12.63, 95% CI = 4.20–38.03), insomnia (OR = 6.26, 95% CI = 2.80–14.01), and loneliness (OR = 3.24, 95% CI = 1.74–6.04) compared to the first cluster. Conclusions These findings firstly clarify the prevalence and correlated factors of CB victimization among employees in Japan. Further, we showed that psychological wellbeing can be impaired by the coexistence of TB and CB. Our research could be the first step to develop the effective countermeasures against workplace CB.

Scd6, a yeast homologue of human RAP55, is a component of messenger ribonucleoproteins (mRNPs) that repress translation by binding to translation initiation factors, and also is a decapping activator along with the binding partners Edc3 and Dhh1. Herein, we report that Scd6 is a substrate of the intrinsic protein arginine methyltransferase, Hmt1, in budding yeast Saccharomyces cerevisiae. Mass spectrometric analysis revealed that several arginine residues within the Scd6 RGG motif, which is important for mRNA binding, were methylated in Hmt1 dependent manner. Under stress conditions such as glucose starvation, Scd6 localized to cytoplasmic processing bodies (P-bodies) wherein translationally repressed mRNPs and untranslated mRNAs accumulate. Localization of Scd6 to P-bodies was impaired in hmt1 deletion mutant and in the presence of methylation-deficient substitution of Scd6. In addition, deletion of scd6 and dhh1 led to severe synthetic growth defect at high temperature. Methylation-deficient mutation of Scd6 suppressed the phenotypic defects of scd6 dhh1 double mutant, whereas methylation-mimic mutation did not, suggesting that the arginine methylation might negatively regulate Scd6 function relating to Dhh1. Therefore, the present data suggest that Hmt1-based arginine methylation is required for Scd6 localization and function.

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Familial thrombocytosis (FT) is a rare, inherited form of myeloproliferative neoplasms (MPN). Germline mutations have been identified mostly in THPO [1] and MPL [2] genes, while only 6 JAK2 germline mutations in 5 families have been reported [3][4][5][6]. In a previous report, all the members of a family affected with the JAK2 R867Q mutation showed thrombocytosis alone with normal hemoglobin levels [6]. Here we