The mechanisms through which bone marrow adipocytes might influence differentiation and function of osteoblasts are not completely understood. To investigate the direct effects of bone marrow fat cells on osteoblast function, an ex vivo co-culture system was utilized comprising either primary fat cells or differentiated 3T3-L1 adipocytes and osteoblastic cells on transwells. In co-culture, both adipocytes and osteoblastic cells were differentiated into adipocytes or osteoblasts, respectively, before culturing on transwells. Co-culture with either primary fat cells or fully differentiated 3T3-L1 adipocytes significantly decreased mRNA and protein expression of runt-related transcription factor 2 (Runx2) in osteoblastic cells. An increase in mRNA and protein expression of peroxisome proliferator-activated receptor γ (PPARγ) occurred concomitantly with the reduction of Runx2 expression. Adiponectin concentration was increased in the media by co-culture. In addition, co-culture with conditioned media from fat cells increased PPARγ promoter activity and decreased Runx2 promoter activity. Knockdown of PPARγ or adiponectin receptor 1 in osteoblastic cells by siRNA prevented the down-regulation of mRNA expression of Runx2 in osteoblastic cells cultured with fully differentiated 3T3-L1 cells. Furthermore, co-transfection with PPARγ decreased Runx2 promoter activity. A marker of osteogenesis, alkaline phosphatase activity in osteoblastic cells was significantly decreased by co-culture. Annexin V/propidium iodide staining showed that co-culture did not induce apoptosis in osteoblastic cells. Thus, we conclude that adipocytes modulate key metabolic functions of osteoblasts through the release of secretory products. PPARγ plays a key role in mediating the effects of adipocytes on osteoblasts.

Members of group III histidine kinases from different filamentous fungi were previously shown to mediate osmoregulation and resistance to dicarboximide, phenylpyrrole and, aromatic hydrocarbon fungicides. In this study, we report the disruption of the gene encoding group III histidine kinase, AlHK1, in the economically important plant pathogen Alternaria longipes. The AlHK1 gene disruption had pleiotropic effects on this fungus. Besides the expected osmosensitivity and fungicides resistance, AlHK1 participated in the spore production process. In addition, the ΔAlHK1 strains had stronger aggressive ability to infect their host plant than that of their parental strain, the wild-type strain C-00, suggested that AlHK1 was involved in the pathogenicity of A. longipes and performed in this function by a negative manner. This is the first report to our knowledge.

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