A syndrome of mutualism reinforces the lifestyle of a sloth

Arboreal herbivory is rare among mammals. The few species with this lifestyle possess unique adaptions to overcome size-related constraints on nutritional energetics. Sloths are folivores that spend most of their time resting or eating in the forest canopy. A three-toed sloth will, however, descend its tree weekly to defecate, which is risky, energetically costly and, until now, inexplicable. We hypothesized that this behaviour sustains an ecosystem in the fur of sloths, which confers cryptic nutritional benefits to sloths. We found that the more specialized three-toed sloths harboured more phoretic moths, greater concentrations of inorganic nitrogen and higher algal biomass than the generalist two-toed sloths. Moth density was positively related to inorganic nitrogen concentration and algal biomass in the fur. We discovered that sloths consumed algae from their fur, which was highly digestible and lipid-rich. By descending a tree to defecate, sloths transport moths to their oviposition sites in sloth dung, which facilitates moth colonization of sloth fur. Moths are portals for nutrients, increasing nitrogen levels in sloth fur, which fuels algal growth. Sloths consume these algae-gardens, presumably to augment their limited diet. These linked mutualisms between moths, sloths and algae appear to aid the sloth in overcoming a highly constrained lifestyle.     

异染色质相关蛋白TRIM28调控锌指蛋白和原钙黏蛋白家族基因的转录

目的 TRIM28是一种异染色质相关蛋白,通过和SETDB1、HP1相互作用参与H3K9me3修饰的建立,本文旨在更深入地研究TRIM28的相关功能。方法 本文利用CRISPR/Cas9技术、染色质免疫共沉淀技术、免疫印迹技术和实时荧光定量PCR技术,建立HEK293F Trim28基因敲除细胞系,分析一系列实验数据结果。结果 Trim28主要抑制内源表达水平较低的基因转录,进一步分析发现Trim28调控锌指蛋白家族基因和原钙黏蛋白β家族基因的转录。在Trim28敲除细胞系中,锌指蛋白家族基因H3K27ac修饰、H3K4me1修饰和H3K4me3修饰都显著上升,H3K9me3修饰下降。原钙黏蛋白β家族基因的H3K4me3修饰显著上升,H3K9me3修饰下降。结论 这些结果提示TRIM28通过改变染色质的开放程度调控锌指蛋白和原钙黏蛋白β家族基因的转录,为更深入研究TRIM28的功能提供了新的思路。     

Paradoxical role of PGE2 and cAMP in Actinobacillus actinomycetemcomitants strain Y4-induced lymphocyte proliferation.

An immune mechanism has been suggested in the pathogenesis of periodontal disease. Actinobacillus actinomycetemcomitants (Aa) has been implicated as one of the etiological agents that induces the major immune response together with a dense infiltrate of inflammatory cells. But the exact role of these immune cells in periodontal disease has not yet been clarified. In this study the T lymphocyte (TL) proliferative response was evaluated after having being exposed to free cell supernatant (SN) from Aa. Aa SN increased TL proliferation. This mitogenic effect of Aa SN was attenuated by pretreating TL with indomethacin (INDO) or acetylsalicylic acid (ASA) but not by polymyxin B. The inhibitory effect of INDO on cell proliferation was reversed by the addition of prostaglandin E2 (PGE2) to the culture assay. Moreover, when immune cells were exposed to Aa SN they were able to generate PGE2 at the same time as intracellular levels of cAMP decreased. Both, PGE2 release and decrease accumulation of cAMP in TL were blunted by treated lymphocytes with INDO. In this paper we demonstrate that cell free SN from Aa induces a mitogenic effect on murine lymphocytes. The mechanism involves the host's immunecompetent cells and the release of PGE2 and appears not to be induced by capsular-like polysaccharide antigen. Results show a paradoxical mitogenic effect of Aa SN accompanied by increased generation of PGE2 and decreased production of cAMP by lymphocytes.     

Allgemeine Physiko-Chemie der Zellen und Gewebe

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Allgemeine Physikochemie der Zellen und Gewebe

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