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Nichols, H.

Publications and source records attributed to Nichols, H..

2 recordsLinked to original sources

Reproductive restraint to avoid the costs of reproductive conflict in a cooperatively breeding mammal

The costs of reproductive conflict can be an important factor shaping the evolution of life histories in animal societies. These costs may change as individuals age and grow, and with within-group competition. Social costs of reproductive conflict have been invoked to explain why females might gain from delaying maturity or ceasing reproduction midway through life, but not in males. Here we analyze more than 20 years of data to understand how individual male banded mongooses adjust their reproductive activity in response to the costs of reproductive conflict. In banded mongooses groups multiple female breeders enter oestrus synchronously and males compete to mate guard the females. The oldest and heaviest males in the group gained the greatest share of paternity, while younger and lighter males obtained little or no paternity. Those lighter males that are reproductively active paid disproportionate survival costs. Our results suggest that by delaying or suppressing reproduction early in life, males may reduce their mortality. Males may also avoid inflicting costs on their male kin by queuing. These results from an egalitarian cooperative breeding mammal may provide a rare example of voluntary reproductive restraint, although we cannot discount reproductive suppression by rival males.

animal behavior and cognition↗

Glucose promotes resistance of human commensal Escherichia coli against contact-killing by pandemic Vibrio cholerae

Evolutionary arms races among organisms are broadly prevalent and bacteria have evolved defensive strategies against various attackers. A common microbial aggression mechanism is the Type VI Secretion System (T6SS), a contact-dependent bacterial weapon used to deliver toxic effector proteins into adjacent target cells. Sibling cells constitutively express immunity proteins that neutralize effectors. However, less is known about mechanisms that allow non-sibling bacteria to respond to external cues and survive T6SS attacks independently of immunity proteins. In this study, we show that resistance to T6SS attacks is promoted by a genetically controlled response to exogenous glucose. We observe that multiple human Escherichia coli commensal strains lacking immunity proteins are sensitive to T6SS attacks from pandemic Vibrio cholerae on nutrient-rich media. By contrast, E. coli cells become resistant to attacks when co-cultured on the same media with glucose. We confirm that glucose does not impair V. cholerae T6SS activity. Instead, we find that cAMP receptor protein (CRP), which alters expression of hundreds of genes in response to glucose, controls resistance to T6SS attacks in E. coli cells. Consistent with the observed resistance on media with glucose, an E. coli crp disruption mutant survives significantly better against V. cholerae T6SS attacks even in the absence of glucose. Finally, we also show that resistance to T6SS attacks depends on the pH of the medium and varies based on the target and killer strains. IMPORTANCEMany Gram-negative bacteria, including important pathogens, encode T6SS genes to deliver toxic effectors and eliminate competitors. Our results uncover a novel defense mechanism against T6SS attacks that is triggered by an external stimulus and mediated by a metabolic response in non-kin target cells. In microbiomes such as those in gastrointestinal tracts where T6SS activity is known to occur, signaling by metabolites like glucose may affect the efficacy of T6SS attacks and alter microbial community composition. Our findings could have vast implications for microbial interactions during pathogen colonization of hosts and survival of bacterial cells in environmental communities. Furthermore, the glucose-mediated resistance observed here might provide a novel example of an evolutionary arms race between killer T6SS cells and target bacteria.

microbiology↗