Optimal window of caloric restriction onset limits its beneficial impact on T‐cell senescence in primates

We have recently shown in non‐human primates that caloric restriction (CR) initiated during adulthood can delay T‐cell aging and preserve naïve CD8 and CD4 T cells into advanced age. An important question is whether CR can be initiated at any time in life, and whether age at the time of onset would modulate the beneficial effects of CR. In the current study, we evaluated the impact of CR started before puberty or during advanced age on T‐cell senescence and compared it to the effects of CR started in early adulthood. Our data demonstrate that the beneficial effects of adult‐onset CR on T‐cell aging were lost by both early and late CR onset. In fact, some of our results suggest that inappropriate initiation of CR may be harmful to the maintenance of T‐cell function. This suggests that there may be an optimal window during adulthood where CR can delay immune senescence and improve correlates of immunity in primates.     

The diversity of mycorrhizal fungi in Japanese Cephalanthera species

The diversity of mycorrhizal fungi among four Japanese Cephalanthera (Orchidaceae) species was examined at a total of seven sites, based on sequence variation in nuclear ribosomal DNA. This is the first report to detect mycorrhizal fungi in C. subaphylla. Two patterns of mycorrhizal associations were confirmed from our results. C. falcata has lower fungal specificity, associating with Russulaceae, Sebacinales and Thelephoraceae. By contrast, the three Cephalanthera species C. erecta, C. subaphylla, and C. longifolia were associated mainly with Thelephoraceae fungi. There is no large difference found in mycobionts between green and albino individuals of C. falcata and no distinct preference of Japanese Cephalanthera species for a specific fungal group of Thelephoraceae.     

Epistemic artefacts: on the uses of complexity in anthropology

Distinctions between the ‘simple’ and the ‘complex’ have enjoyed a long and varied career in anthropology. Simplicity was once part of a collective fantasy about what life was like elsewhere, tingeing studies of tribal life with human longing for simpler ways of being. With the reflexive turn and the rise of cultural critique, simplicity has been all but excommunicated in favour of widespread diagnoses of complexity. In this article, I tease out some transformations in the uses of complexity in anthropology, and weave in some critical responses to these uses, spanning many decades, from within the discipline. I pay special attention to recent critiques by anthropologists who are beginning to grow weary of complexity as both an end‐in‐itself for scholarship and an empirical diagnosis. For these critics, complexity is deeply entwined with anthropological methods and knowledge practices. Drawing on these critical views, I suggest that complexity may be an epistemological artefact, rather than something that can be diagnosed ‘out there’, and offer a way of reframing complexity as a ‘dominant problematic’ in anthropology and beyond.     

Carrying capacity in a heterogeneous environment with habitat connectivity

A large body of theory predicts that populations diffusing in heterogeneous environments reach higher total size than if non‐diffusing, and, paradoxically, higher size than in a corresponding homogeneous environment. However, this theory and its assumptions have not been rigorously tested. Here, we extended previous theory to include exploitable resources, proving qualitatively novel results, which we tested experimentally using spatially diffusing laboratory populations of yeast. Consistent with previous theory, we predicted and experimentally observed that spatial diffusion increased total equilibrium population abundance in heterogeneous environments, with the effect size depending on the relationship between r and K. Refuting previous theory, however, we discovered that homogeneously distributed resources support higher total carrying capacity than heterogeneously distributed resources, even with species diffusion. Our results provide rigorous experimental tests of new and old theory, demonstrating how the traditional notion of carrying capacity is ambiguous for populations diffusing in spatially heterogeneous environments.     

Weak cell cycle dependency but strong distortive effects of transfection with Lipofectamine 2000 in near‐physiologically synchronized cell culture

Previously, we reported a method to generate and validate cell cycle‐synchronized cultures of multiple mammalian suspension cell lines under near‐physiological conditions. This method was applied to elucidate the putative interdependencies of the cell cycle and recombinant protein expression in the human producer cell line HEK293s using Lipofectamine 2000 and the reporter plasmid pcDNA3.3 enhanced green fluorescent protein, destabilized using PEST sequence. A population‐resolved modeling approach was applied to quantitatively assess putative variations of cell cycle dependent expression rates based on the obtained experimental data. We could not confirm results published earlier by other groups, based on nonphysiological synchronization attempts, reporting transfection efficiency being strongly dependent on the cell cycle phase at transfection time point. On the other hand, it is demonstrated that transfection and protein expression distort the progression of the cell cycle.     

Antibody fingerprints in lyme disease deciphered with high density peptide arrays

Lyme disease is the most common tick‐borne infectious disease in Europe and North America. Previous studies discovered the immunogenic role of a surface‐exposed lipoprotein (VlsE) of Borreliella burgdorferi. We employed high density peptide arrays to investigate the antibody response to the VlsE protein in VlsE‐positive patients by mapping the protein as overlapping peptides and subsequent in‐depth epitope substitution analyses. These investigations led to the identification of antibody fingerprints represented by a number of key residues that are indispensable for the binding of the respective antibody. This approach allows us to compare the antibody specificities of different patients to the resolution of single amino acids. Our study revealed that the sera of VlsE‐positive patients recognize different epitopes on the protein. Remarkably, in those cases where the same epitope is targeted, the antibody fingerprint is almost identical. Furthermore, we could correlate two fingerprints with human autoantigens and an Epstein‐Barr virus epitope; yet, the link to autoimmune disorders seems unlikely and must be investigated in further studies. The other three fingerprints are much more specific for B. burgdorferi. Since antibody fingerprints of longer sequences have proven to be highly disease specific, our findings suggest that the fingerprints could function as diagnostic markers that can reduce false positive test results.     

Cutting edge: Chk1 directs senescence and mitotic catastrophe in recovery from G2 checkpoint arrest

Besides the well‐understood DNA damage response via establishment of G₂ checkpoint arrest, novel studies focus on the recovery from arrest by checkpoint override to monitor cell cycle re‐entry. The aim of this study was to investigate the role of Chk1 in the recovery from G₂ checkpoint arrest in HCT116 (human colorectal cancer) wt, p53^–/– and p21^–/– cell lines following H₂O₂ treatment. Firstly, DNA damage caused G₂ checkpoint activation via Chk1. Secondly, overriding G₂ checkpoint led to (i) mitotic slippage, cell cycle re‐entry in G₁ and subsequent G₁ arrest associated with senescence or (ii) premature mitotic entry in the absence of p53/p21^WAF1 causing mitotic catastrophe. We revealed subtle differences in the initial Chk1‐involved G₂ arrest with respect to p53/p21^WAF1: absence of either protein led to late G₂ arrest instead of the classic G₂ arrest during checkpoint initiation, and this impacted the release back into the cell cycle. Thus, G₂ arrest correlated with downstream senescence, but late G₂ arrest led to mitotic catastrophe, although both cell cycle re‐entries were linked to upstream Chk1 signalling. Chk1 knockdown deciphered that Chk1 defines long‐term DNA damage responses causing cell cycle re‐entry. We propose that recovery from oxidative DNA damage‐induced G₂ arrest requires Chk1. It works as cutting edge and navigates cells to senescence or mitotic catastrophe. The decision, however, seems to depend on p53/p21^WAF1. The general relevance of Chk1 as an important determinant of recovery from G₂ checkpoint arrest was verified in HT29 colorectal cancer cells.