Braeckman BP et al. (2002) Aging Cell "Rebuttal to Van Voorhies: 'the influence of metabolic rate on longevity in the nematode Caenorhabditis elegans'."

Braeckman BP, Houthoofd K, Vanfleteren JR

[Aging Cell, 2002]

The papers by Van Voorhies in Free Radical Biology & Medicine (33, 587-596, 2002) and in this journal claim that the major longevity-extending mutations in C. elegans essentially act by reducing metabolic rate as predicted by the rate-of-living theory, and do not alter any metabolically independent mechanism specific to aging. In contrast, we found no evidence of a reduction in metabolic rate in these mutants using different experimental approaches. Now, Van Voorhies challenges the accuracy of our experimental results.

Dehn AS et al. (2022) PLoS Biol "Binucleation ramps up gene expression meeting the physiological demands of an organism."

Dehn AS, Losick VP

[PLoS Biol, 2022]

In this issue of PLOS Biology, van Rijnberk and colleagues show how polyploidy, via binucleation, enables Caenorhabditis elegans intestinal cells to ramp up gene expression supplying the oocytes with the necessary lipids for optimal organismal growth and reproductive fitness.

Sendinc E et al. (2015) Cell "Remodeling Your Way out of Cell Cycle."

Sendinc E, Shi Y, Jambhekar A

[Cell, 2015]

Throughout development, proliferative progenitors lose their mitotic potential, exit the cell cycle, and differentiate. In this issue, Ruijtenberg and van den Heuvel identify an important lineage-specific role for a SWI/SNF chromatin-remodeling complex that collaborates with core cell-cycle regulators to promote cell-cycle exit and terminal muscle cell differentiation.

Partridge L et al. (1992) Nature "Evolutionary biology. What the sperm count costs."

Partridge L, Harvey PH

[Nature, 1992]

Dissecting the sex life of the nematode worm Caenorhabditis elegans has already provided surprises for biologists interested in life-history theory. In a report on page 456 of this issue, Van Voorhies throws another spanner in the works by demonstrating that the costs of producing sperm are not as negligible as we might have thought.

Labouesse M (2015) Dev Cell "Adhesion with a Sumo."

Labouesse M

[Dev Cell, 2015]

Adherens junctions (AJs) play a crucial role in epithelial tissue development and tumorigenesis, and the mechanisms controlling their assembly and disassembly have therefore attracted considerable attention. A paper from Tsur et al. (2015) in this issue of Developmental Cell now shows how sumoylation and desumoylation of E-cadherin promotes its recruitment to AJs.

Storelli G et al. (2013) Cell Metab "Metformin, microbes, and aging."

Leulier M, Storelli G, Tefit M

[Cell Metab, 2013]

The mechanisms underlying the biological activity of metformin, a widely prescribed drug to treat type 2 diabetes, remain elusive. In a recent issue of Cell, Cabreiro et al. report that in C. elegans, metformin indirectly impacts lifespan by altering the methionine metabolism of its microbial partner E. coli (Cabreiro et al., 2013).

Nguyen TP et al. (2012) BMC Biol "Folate status of gut microbiome affects Caenorhabditis elegans lifespan."

Clarke CF, Nguyen TP

[BMC Biol, 2012]

In a paper in BMC Biology Virk et al. show that Caenorhabditis elegans lifespan is extended in response to a diet of folate-deficient Escherichia coli. The deficiencies in folate biosynthesis were due to an aroD mutation, or treatment of E. coli with sulfa drugs, which are mimics of the folate precursor para-aminobenzoic acid. This study suggests that pharmacological manipulation of the gut microbiome folate status may be a viable approach to slow animal aging, and raises questions about folate supplementation.

Van Voorhies WA (2002) Aging Cell "Rebuttal to Braeckman et al: 'Assessing metabolic activity in again Caenorhabditis elegans: concepts and controversies'."

Van Voorhies WA

[Aging Cell, 2002]

The reviews by Braechman et al. and Van Voorhies in this issue of Aging Cell concur on the potential importance of metabolic rate and function to longevity in C. elegans. These reviews differ though, on their assessment of whether long-lived C. elegans mutants have a reduced metabolic rate compared to wild-type worms. At the centre of this disagreement are two main issues: the importance of measurement conditions when conducting metabolic assays on C. elegans, and which techniques are appropriate for measuring the metabolic rate of an organism and subsequent analysis of such data. These issues are interconnected; if the conditions under which an organism's metabolic rate are measured have a large impact on the resulting data, conclusions drawn from data collected from animals under different conditions may be invalid irrespective of the validity of the measurement methods. Conversely, measurement techniques which produce spurious data cannot be used to draw accurate conclusions about the metabolic rate of an organism, regardless of the conditions under which the organism was maintained.

Garsin DA et al. (2013) Gut Microbes "Candida albicans and Enterococcus faecalis in the gut: synergy in commensalism?"

Garsin DA, Lorenz MC

[Gut Microbes, 2013]

The fungus Candida albicans and the gram-positive bacterium Enterococcus faecalis are both normal residents of the human gut microbiome and cause opportunistic disseminated infections in immunocompromised individuals. Using a nematode infection model, we recently showed that co-infection resulted in less pathology and less mortality than infection with either species alone and this was partly explained by an interkingdom signaling event in which a bacterial-derived product inhibits hyphal morphogenesis of C. albicans. In this addendum we discuss these findings in the contest of other described bacterial-fungal interactions and recent data suggesting a potentially synergistic relationship between these two species in the mouse gut as well. We suggest that E. faecalis and C. albicans promote a mutually beneficial association with the host, in effect choosing a commensal lifestyle over a pathogenic one.

Sewell AK et al. (2018) Microb Cell "An unexpected benefit from E. coli: how enterobactin benefits host health."

Qi B, Han M, Sewell AK

[Microb Cell, 2018]

Iron plays many critical roles in human biology, such as aiding the transport of oxygen and mediating redox reactions. Iron is essential for life, yet little is known about how iron is taken up into mitochondria to impact the labile iron pool. Iron deficiency is one of the most prevalent human nutrient-deficiency diseases in the world and is a major cause of anemia that affects &gt;25% of the world's population, but unfortunately the current treatment (oral iron supplementation) is inefficient and has many side effects. A greater understanding of iron uptake, and discovery of molecules that aid in this process, may lead to more effective treatments for iron deficiency. In this study, we uncovered a unique and surprising role for an <i>Escherichia coli</i>-produced siderophore enterobactin (Ent) that facilitates iron uptake by the host, observed in both <i>C. elegans</i> and mammalian cells. Although siderophores are well-known Fe⁺³ scavengers, this activity has previously been described to only benefit iron acquisition by bacteria, not the host. This unexpected function is dependent on the binding of Ent to the host's ATP synthase -subunit but is independent of other subunits of the ATP synthase. This finding marks a major shift regarding the role of this siderophore in the &quot;iron tug-of-war&quot; paradigm, which is often used to describe the fight between the bacteria and the host for this essential micronutrient. Instead, this study presents <i>E. coli</i> as a commensal &quot;friend&quot; that provides a molecule that supports the host's iron homeostasis. This work reveals a novel, beneficial role of a bacteria-generated molecule in aiding the host's iron homeostasis, and points to surprising new benefits from commensal bacteria.