Role of Prohibitins in Aging and Therapeutic Potential Against Age-Related Diseases

A decline in mitochondrial function has long been associated with age-related health decline. Several lines of evidence suggest that interventions that stimulate mitochondrial autophagy (mitophagy) can slow aging and prolong healthy lifespan. Prohibitins (PHB1 and PHB2) assemble at the mitochondrial inner membrane and are critical for mitochondrial homeostasis. In addition, prohibitins (PHBs) have diverse roles in cell and organismal biology. Here, we will discuss the role of PHBs in mitophagy, oxidative phosphorylation, cellular senescence, and apoptosis. We will also discuss the role of PHBs in modulating lifespan. In addition, we will review the links between PHBs and diseases of aging. Finally, we will discuss the emerging concept that PHBs may represent an attractive therapeutic target to counteract aging and age-onset disease.

Development of an Online General Biology Open Educational Resource (OER) Laboratory Manual

Currently, many academic institutions are using one or more variations of online modalities due to the COVID-19 pandemic, and science educators face a unique challenge with distance-learning laboratories. Many resources to engage students in virtual, interactive laboratory activities exist, but we found that high costs and/or overlooked content left gaps for several topics typically taught in a general, introductory biology course for undergraduate biology majors (e.g., organismal biology).

Phyloreferences: Tree-Native, Reproducible, and Machine-Interpretable Taxon Concepts

Evolutionary and organismal biology, similar to other fields in biology, have become inundated with data. At the same rate, we are experiencing a surge in broader evolutionary and ecological syntheses for which tree-thinking is the staple for a variety of post-tree analyses. To fully take advantage of this wealth of data to discover and understand large-scale evolutionary and ecological patterns, computational data integration, i.e. the use of machines to link data at large scale by shared entities, is crucial. The most common shared entity by which evolutionary and ecological data need to be linked is the taxon to which they belong. In this paper, we propose a set of requirements that a system for defining such taxa should meet for computational data science: taxon definitions should maintain conceptual consistency, be reproducible via a known algorithm, be computationally automatable, and be applicable across the tree of life. We argue that Linnaean names based in Linnaean taxonomy, by far the most prevalent means of linking data to taxa, fail to meet these requirements due to fundamental theoretical and practical shortfalls. We argue that for the purposes of data-integration we should instead use phylogenetic clade definitions transformed into formal logic expressions. We call such expressions phyloreferences, and argue that, unlike Linnaean names, they meet all requirements for effective data-integration.

Erratum

Erratum to: Exceptional changes in skeletal anatomy under domestication: the case of brachycephaly Integrative Organismal Biology, Volume 3, Issue 1, 2021, obab023, https://doi.org/10.1093/iob/obab023 Due to production error in the above article, figure 1 has been updated as follows online:

The genetic paradigms of dietary restriction fail to extend life span in cep-1(gk138) mutant of C. elegans p53 due to possible background mutations

Dietary restriction (DR) increases life span and improves health in most model systems tested, including non-human primates. In C. elegans, as in other models, DR leads to reprogramming of metabolism, improvements in mitochondrial health, large changes in expression of cytoprotective genes and better proteostasis. Understandably, multiple global transcriptional regulators like transcription factors FOXO/DAF-16, FOXA/PHA-4, HSF1/HSF-1 and NRF2/SKN-1 are important for DR longevity. Considering the wide-ranging effects of p53 on organismal biology, we asked whether the C. elegans ortholog, CEP-1 is required for DR-mediated longevity assurance. We employed the widely-used TJ1 strain of cep-1(gk138). We show that cep-1(gk138) suppresses the life span extension of two genetic paradigms of DR, but two non-genetic modes of DR remain unaffected in this strain. We find that two aspects of DR, increased autophagy and up-regulation of the expression of cytoprotective xenobiotic detoxification program (cXDP) genes, are dampened in cep-1(gk138). Importantly, we find that background mutation(s) in the strain may be the actual cause for the phenotypic differences that we observed and cep-1 may not be directly involved in genetic DR-mediated longevity assurance in worms. Identifying these mutation(s) may reveal a novel regulator of longevity required specifically by genetic modes of DR.

The genetic paradigms of dietary restriction fail to extend life span in cep-1(gk138) mutant of C. elegans p53 due to possible background mutations

Dietary restriction (DR) increases life span and improves health in most model systems tested, including non-human primates. In C. elegans, as in other models, DR leads to reprogramming of metabolism, improvements in mitochondrial health, large changes in gene expression, including increase in expression of cytoprotective genes, better proteostasis etc. Understandably, multiple global transcriptional regulators like transcription factors FOXO/DAF-16, FOXA/PHA-4, HSF1/HSF-1 and NRF2/SKN-1 are important for DR longevity. Considering the wide-ranging effects of p53 on organismal biology, we asked whether the C. elegans ortholog, CEP-1 is required for DR-mediated longevity assurance. We employed the widely-used TJ1 strain of cep-1(gk138). We show that cep-1(gk138) suppresses the life span extension of two genetic paradigms of DR, but two non-genetic modes of DR remain unaffected in this strain. We find that in cep-1(gk138), two aspects of DR, increased autophagy and the up-regulation of expression of cytoprotective xenobiotic detoxification program (cXDP) genes are dampened. Importantly, we find that background mutation(s) in the strain may be the actual cause for the phenotypic differences that we observed and cep-1 may not be directly involved in genetic DR-mediated longevity assurance in worms. Identifying these mutation(s) may reveal a novel regulator of longevity required specifically by genetic modes of DR.