The autophagy-related gene Atg101 in Drosophila regulates both neuron and midgut homeostasis.

Atg101 is an autophagy-related gene identified in worms, flies, mice, and mammals, which encodes a protein that functions in autophagosome formation by associating with the ULK1-Atg13-Fip200 complex. In the last few years, the critical role of Atg101 in autophagy has been well-established through biochemical studies and the determination of its protein structure. However, Atg101's physiological role, both during development and in adulthood, remains less understood. Here, we describe the generation and characterization of an Atg101 loss-of-function mutant in Drosophila and report on the roles of Atg101 in maintaining tissue homeostasis in both adult brains and midguts. We observed that homozygous or hemizygous Atg101 mutants were semi-lethal, with only some of them surviving into adulthood. Both developmental and starvation-induced autophagy processes were defective in the Atg101 mutant animals, and Atg101 mutant adult flies had a significantly shorter lifespan and displayed a mobility defect. Moreover, we observed the accumulation of ubiquitin-positive aggregates in Atg101 mutant brains, indicating a neuronal defect. Interestingly, Atg101 mutant adult midguts were shorter and thicker and exhibited abnormal morphology with enlarged enterocytes. Detailed analysis also revealed that the differentiation from intestinal stem cells to enterocytes was impaired in these midguts. Cell type-specific rescue experiments disclosed that Atg101 had a function in enterocytes and limited their growth. In summary, the results of our study indicate that Drosophila Atg101 is essential for tissue homeostasis in both adult brains and midguts. We propose that Atg101 may have a role in age-related processes.

Chryseobacterium lineare sp. nov., isolated from a limpid stream.

A Gram-stain-negative, aerobic, non-motile, rod-shaped, yellow-pigmented bacterial strain, XC0022T, isolated from freshwater of a limpid stream in Zhejiang, China, was studied using a polyphasic approach. The phylogenetic analysis based on 16S rRNA gene sequences clearly showed an allocation to the genus Chryseobacterium with the highest sequence similarities of 98.0 % to Chryseobacterium taeanense PHA3-4T, 97.2 % to Chryseobacterium taihuense THMBM1T, 97.1 % to Chryseobacterium rigui CJ16T and 97.1 % to Chryseobacteriumprofundimaris DY46T. 16S rRNA gene sequence similarities to all other species of the genus Chryseobacterium were below 97.0 % (92.3-96.8 %). DNA-DNA hybridization results showed that strain XC0022T was 55.3 %, 49.8 % and 31.1 % related to C. taeanense DSM 17071T, Chryseobacteriumtaichungense DSM 17453T and Chryseobacteriumgleum JCM 2410T, respectively. The quinone system was composed only of MK-6. Strain XC0022T possessed iso-C15 : 0, iso-C17 : 0 3-OH, C18 : 1ω9c and summed feature 3 (iso-C15 : 0 2-OH/C16 : 1ω7c) as the major fatty acids. The polar lipids profile consisted of one phosphatidylethanolamine, one unidentified glycolipid, four unidentified aminolipids and two unidentified lipids. The G+C content of the genomic DNA was 29.7 mol%. On the basis of phenotypic, phylogenetic and chemotaxonomic data, strain XC0022T (=KCTC 52364T=MCCC 1K02723T) represents a novel species of the genus Chryseobacterium, for which the name Chryseobacterium lineare sp. nov. is proposed.

A Novel Neuroprotective Role of Phosphatase of Regenerating Liver-1 against CO2 Stimulation in Drosophila.

Neuroprotection is essential for the maintenance of normal physiological functions in the nervous system. This is especially true under stress conditions. Here, we demonstrate a novel protective function of PRL-1 against CO2 stimulation in Drosophila. In the absence of PRL-1, flies exhibit a permanent held-up wing phenotype upon CO2 exposure. Knockdown of the CO2 olfactory receptor, Gr21a, suppresses the phenotype. Our genetic data indicate that the wing phenotype is due to a neural dysfunction. PRL-1 physically interacts with Uex and controls Uex expression levels. Knockdown of Uex alone leads to a similar wing held-up phenotype to that of PRL-1 mutants. Uex acts downstream of PRL-1. Elevated Uex levels in PRL-1 mutants prevent the CO2-induced phenotype. PRL-1 and Uex are required for a wide range of neurons to maintain neuroprotective functions. Expression of human homologs of PRL-1 could rescue the phenotype in Drosophila, suggesting a similar function in humans.