Outplanting of branching Acropora enhances recolonization of a fish species and protects massive corals from predation

Damselfish of the genus Stegastes inhabit territories and cultivate algal gardens on branching corals of the genus Acropora, aggressively protecting their territories from other fish and preventing predation upon corals within the territory. This behaviour has important ecological impacts and could also be useful in reducing predation on outplanted corals during reef restoration efforts. However, the degree of protection from predators may depend on the ability of Stegastes spp. to recolonise outplanted or newly established coral colonies. Protection of bleaching-resilient massive corals within territories may be of particular importance due to the role of these corals in maintaining coral cover following bleaching events. This study examined whether the presence of Stegastes spp. reduces predation on the massive bleaching-resilient coral Porites lutea in the Mauritian lagoon, and whether Stegastes spp. readily colonise outplanted branching coral fragments and provide adjacent massive corals with indirect protection from predation. Predation levels on wild-occurring and outplanted P. lutea within and outside Stegastes spp. territories were measured. In addition, Acropora muricata branches were outplanted adjacent to wild P. lutea colonies outside Stegastes spp. territories, and recolonisation of these outplants by Stegastes spp. and the impacts of recolonisation on predation were monitored. Both wild and outplanted P. lutea colonies within Stegastes spp. territories sustained less predation damage compared to colonies outside territories. Stegastes spp. recolonized outplanted A. muricata colonies within six months of outplanting, and in doing so returned predation protection to adjacent P. lutea colonies. The ability of Stegastes spp. to colonise outplanted corals and provide indirect protection to adjacent massive bleaching-resilient corals may inform coral outplanting efforts in systems where Stegastes spp. are common. Encouraging Stegastes spp. recolonisation may help to reduce predation damage to corals within territories and potentially improve the success of rehabilitation efforts.

     

Genes for basement membrane proteins are coordinately expressed in differentiating F9 cells but not in normal adult murine tissues

We have obtained cDNA clones coding for the A, B1, and B2 chains of laminin by screening a cDNA library prepared from mouse EHS tumor poly(A)RNA in the lambda gt11 expression vector with polyclonal antibody against denatured laminin. These cDNA clones were used in combination with a cDNA clone coding for the alpha 1 type IV collagen chain to study the regulation of genes for these basement membrane proteins in retinoic acid-induced differentiating mouse F9 teratocarcinoma cells and in various adult murine tissues. The levels of mRNA for the laminin A, B1, and B2 chains and for the alpha 1 type IV collagen chain were increased simultaneously and reached a maximum at almost the same time during the differentiation of F9 cells, suggesting coordinate expression in these cells. The tissue levels of mRNA encoding for the basement membrane components, however, varied considerably. The highest level of the B1 chain mRNA was observed in kidney, whereas, the levels of mRNA for A and B2 chains were highest in heart. Almost the same levels of expression of the alpha 1(IV) collagen mRNA were found in kidney, lung, and heart. The results indicate that the expression of genes for the basement membrane proteins is not coordinately regulated in these tissues. It is thus possible that different subunit structures of the laminin molecule may exist in tissues.     

T-helper 17 cell cytokines and interferon type I: partners in crime in systemic lupus erythematosus?

Introduction

A hallmark of systemic autoimmune diseases like systemic lupus erythematosus (SLE) is the increased expression of interferon (IFN) type I inducible genes, so-called IFN type I signature. Recently, T-helper 17 subset (Th17 cells), which produces IL-17A, IL-17F, IL-21, and IL-22, has been implicated in SLE. As CCR6 enriches for Th17 cells, we used this approach to investigate whether CCR6⁺ memory T-helper cells producing IL-17A, IL-17F, IL-21, and/or IL-22 are increased in SLE patients and whether this increase is related to the presence of IFN type I signature.

Methods

In total, 25 SLE patients and 15 healthy controls (HCs) were included. SLE patients were divided into IFN type I signature-positive (IFN⁺) (n = 16) and negative (IFN^-) (n = 9) patients, as assessed by mRNA expression of IFN-inducible genes (IFIGs) in monocytes. Expression of IL-17A, IL-17F, IL-21, and IL-22 by CD4⁺CD45RO⁺CCR6⁺ T cells (CCR6⁺ cells) was measured with flow cytometry and compared between IFN⁺, IFN^- patients and HCs.

Results

Increased percentages of IL-17A and IL-17A/IL-17F double-producing CCR6⁺ cells were observed in IFN⁺ patients compared with IFN^- patients and HCs. IL-17A and IL-17F expression within CCR6⁺ cells correlated significantly with IFIG expression. In addition, we found significant correlation between B-cell activating factor of the tumor necrosis family (BAFF)–a factor strongly correlating with IFN type I - and IL-21 producing CCR6⁺ cells.

Conclusions

We show for the first time higher percentages of IL-17A and IL-17A/IL-17F double-producing CCR6⁺ memory T-helper cells in IFN⁺ SLE patients, supporting the hypothesis that IFN type I co-acts with Th17 cytokines in SLE pathogenesis.