The transcription factor MAFB is an important regulator of the development and differentiation of various organs and tissues. Previous studies have shown that MAFB is expressed in embryonic and adult mouse testes and is expected to act as the downstream target of retinoic acid (RA) to initiate spermatogenesis. However, its exact localization and function remain unclear. Here, we localized MAFB expression in embryonic and adult testes and analyzed its gene function using Mafb-deficient mice. We found that MAFB and c-MAF are the only large MAF transcription factors expressed in testes, while MAFA and NRL are not. MAFB was localized in Leydig and Sertoli cells at embryonic day (E) 18.5 but in Leydig cells, Sertoli cells, and pachytene spermatocytes in adults. Mafb-deficient testes at E18.5 showed fully formed seminiferous tubules with no abnormal structure or differences in testicular somatic cell numbers compared with those of control wild-type mice. Additionally, the expression levels of genes related to development and function of testicular cells were unchanged between genotypes. In adults, the expression of MAFB in Sertoli cells was shown to be stage specific and induced by RA. By generating Mafb^fl/fl CAG-CreER^™ (Mafb-cKO) mice, in which Cre recombinase was activated upon tamoxifen treatment, we found that the neonatal cKO mice died shortly upon Mafb deletion, but adult cKO mice were alive upon deletion. Adult cKO mice were fertile, and spermatogenesis maintenance was normal, as indicated by histological analysis, hormone levels, and germ cell stage-specific markers. Moreover, there were no differences in the proportion of seminiferous stages between cKO mice and controls. However, RNA-Seq analysis of cKO Sertoli cells revealed that the down-regulated genes were related to immune function and phagocytosis activity but not spermatogenesis. In conclusion, we found that MAFB is dispensable for fetal testis morphogenesis and spermatogenesis maintenance in adult mice, despite the significant gene expression in different cell types, but MAFB might be critical for phagocytosis activity of Sertoli cells.

Type 1 diabetes (T1D) is a chronic autoimmune disease that results from destruction of pancreatic β-cells. T1D subjects were recently shown to harbor distinct intestinal microbiome profiles. Based on these findings, the role of gut bacteria in T1D is being intensively investigated. The mechanism connecting intestinal microbial homeostasis with the development of T1D is unknown. Specific gut bacteria such as Bacteroides dorei (BD) and Ruminococcus gnavus (RG) show markedly increased abundance prior to the development of autoimmunity. One hypothesis is that these bacteria might traverse the damaged gut barrier, and their constituents elicit a response from human islets that causes metabolic abnormalities and inflammation. We have tested this hypothesis by exposing human islets to BD and RG in vitro, after which RNA-Seq analysis was performed. The bacteria altered expression of many islet genes. The commonly upregulated genes by these bacteria were cytokines, chemokines and enzymes, suggesting a significant effect of gut bacteria on islet antimicrobial and biosynthetic pathways. Additionally, each bacteria displayed a unique set of differentially expressed genes (DEGs). Ingenuity pathway analysis of DEGs revealed that top activated pathways and diseases included TREM1 signaling and inflammatory response, illustrating the ability of bacteria to induce islet inflammation. The increased levels of selected factors were confirmed using immunoblotting and ELISA methods. Our data demonstrate that islets produce a complex anti-bacterial response. The response includes both symbiotic and pathogenic aspects. Both oxidative damage and leukocyte recruitment factors were prominent, which could induce beta cell damage and subsequent autoimmunity.

Background: Gallinula chloropus (Linnaeus, 1758) is a wild aquatic omnivorous bird characterized by a marked resistance to harsh environmental conditions and a worldwide distribution. In this study, anatomical, morphometrical, histochemical, and immunohistochemical techniques were employed to study the structure of the gastrointestinal tract of Gallinula chloropus. Results: The esophagus appeared tubular with no distinct crop. Both superficial (SPG) and deep (DPG) proventricular glands were present. The DPG filled about two-thirds of the total wall thickness. Histochemically, the mucosubstances revealed mixed alcian blue-PAS positive reactions. They were mainly localized in the acini of the esophageal glands and SPG, gastric surface epithelium, duct system of DPG, and intestinal goblet cells. The highest number of goblet cells per every 1 mm² of the intestinal mucosa was seen within the ileum and rectum, 2555 ± 468 and 2607 ± 653 respectively. Notably, glucagon immunoreactive (IR) cells were abundant in the mucosa of the small and large intestines and the proventriculus, while somatostatin IR cells were concentrated within the acini of the DPG. IR cells for the mitosis marker phospho-histone H3 (PHH3) were highest within the entire intestinal crypts and mucosa-associated lymphoid tissues (MALT). In contrast, cells IR for the apoptosis marker C.CASP3 were remarkable in epithelial cells at the tips of intestinal villi and in MALT, reflecting the dynamic nature of the latter mentioned structures. Conclusions: The findings of the present study advance our knowledge of the gross and microscopic anatomy of the gastrointestinal tract in wild birds and could help to enhance the productivity of Aves via improving gut health.

The transcription factor c-Maf is a member of the large Maf family, members of which possess transactivation and bZIP domains. c-Maf plays an important role in lens formation, T-lymphocyte differentiation, hypertrophic chondrocyte differentiation, and kidney development in mouse embryos. However, because homozygous deletion of c-Maf in C57BL/6J mice causes embryonic lethality, the functions of c-Maf in adult mice remain largely uninvestigated. To address this issue, we generated c-Maf floxed (c-Maffl/fl) C57BL/6J mice and established tamoxifen-inducible c-Maf knockout mice (c-Maffl/fl; CAG-Cre-ERTMmice, c-MafΔTAM). After tamoxifen injection, adult c-MafΔTAMmice showed successful deletion of c-Maf protein and developed severe cataracts; cataracts are also seen in human patients who have mutations in the c-MAF DNA binding domain. Furthermore, adult c-MafΔTAMmice exhibited abnormal lens structure and impaired differentiation of lens fiber cells. In summary, we established c-Maffl/fland c-MafΔTAMC57BL/6J mice, which can be useful animal models for the investigation of c-Maf function in various developmental stages and can also be used as a disease model for cataracts.