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The mechanisms of microalgal senescence may play an important role in nutrient recycling and enhanced survival. However, the aging physiology of microalgae is an understudied phenomenon. To investigate the patterns of conditional senescence in Chlamydomonas reinhardtii P. A. Dangeard, we used a cell wall-less strain, transformed with a reporter gene to infer changes in photosynthetic gene expression. We examined plastid ultrastructure, photosynthetic function, and photoprotective mechanisms during aging in batch cultures. LHCII transcription levels decreased before the population entered stationary phase, and the characteristic transcriptional light-shift response was lost. A decline in photosynthetic proteins with a concomitant increase in the photoprotective protein, LHCSR, was observed over time. However, nonphotochemical quenching remained stable during growth and stationary phase, and then declined as alternative quenching mechanisms were up-regulated. Photosynthetic efficiency declined, while Fv/Fm remained stable until the death phases. As the culture progressed through stationary phase, disorganization of the chloroplast was observed along with an increase in cytoplasmic oil bodies. We also observed a partial recovery of function and proteins during the final death phase, and attribute this to the release of nutrients into the medium from cell lysis and/or active secretion while cells were senescing. Allowing open gas exchange resulted in high levels of sustained starch production and maintained maximum cell density, prolonging the stationary phase. [ABSTRACT FROM AUTHOR]

Key points: Contraction‐mediated blunting of postjunctional α‐adrenergic vasoconstriction (functional sympatholysis) is attenuated in skeletal muscle of ageing males, brought on by altered postjunctional α1‐ and α2‐adrenergic receptor sensitivity. The extent to which postjunctional α‐adrenergic vasoconstriction occurs in the forearms at rest and during exercise in postmenopausal women remains unknown. The novel findings indicate that contraction‐mediated blunting of α1‐ (via intra‐arterial infusion of phenylephrine) but not α2‐adrenergic (via intra‐arterial infusion of dexmedetomidine) vasoconstriction was attenuated in postmenopausal women compared to young women. Additional important findings revealed that postjunctional α‐adrenergic vasoconstrictor responsiveness at rest does not appear to be affected by age in women. Collectively, these results contribute to our understanding of local neurovascular control at rest and during exercise with age in women. Abstract: Contraction‐mediated blunting of postjunctional α‐adrenergic vasoconstriction (functional sympatholysis) is attenuated in older males; however, direct confirmation of this effect remains unknown in postmenopausal women (PMW). The present study examined whether PMW exhibit augmented postjunctional α‐adrenergic receptor vasoconstriction at rest and during forearm exercise compared to young women (YW). Eight YW (24 ± 1 years) and eight PMW (65 ± 1 years) completed a series of randomized experimental trials: (1) at rest, (2) under high flow (adenosine infusion) conditions and (3) during 6 min of forearm exercise at relative (20% of maximum) and absolute (7 kg) intensities. Phenylephrine (α1‐agonist) or dexmedetomidine (α2‐agonist) was administered during the last 3 min of each trial to elicit α‐adrenergic vasoconstriction. Forearm vascular conductance (FVC) was calculated from blood flow and blood pressure. Vasoconstrictor responsiveness was identified as the change in FVC (%) during α‐adrenergic agonist infusions from baseline (resting trial) or from steady‐state conditions (high flow and exercise trials). During resting and high flow trials, the %FVC during α1‐ and α2‐agonist stimulation was similar between YW and PMW. During exercise, α1‐mediated vasoconstriction was blunted in YW vs. PMW at relative (−6 ± 2% vs. −15 ± 3%) and absolute (−4 ± 2% vs. −14 ± 5%) workloads, such that blood flow and FVC were lower in PMW (P < 0.05 for all). Conversely, α2‐mediated vasoconstriction was similar between YW and PMW at relative (−22 ± 3% vs. −22 ± 4%; P > 0.05) and absolute (−19 ± 3% vs. ‐18 ± 4%; P > 0.05) workloads. Collectively, these findings demonstrate that despite similar α‐adrenergic vasoconstrictor responsiveness at rest, PMW have a decreased ability to attenuate α1‐adrenergic vasoconstriction in contracting skeletal muscle. [ABSTRACT FROM AUTHOR]

Summary: The neuromuscular junction (NMJ) is responsible for transforming nervous system signals into motor behavior and locomotion. In the fruit fly Drosophila melanogaster, an age‐dependent decline in motor function occurs, analogous to the decline experienced in mice, humans, and other mammals. The molecular and cellular underpinnings of this decline are still poorly understood. By specifically profiling the transcriptome of Drosophila motor neurons across age using custom microarrays, we found that the expression of the matrix metalloproteinase 1 (dMMP1) gene reproducibly increased in motor neurons in an age‐dependent manner. Modulation of physiological aging also altered the rate of dMMP1 expression, validating dMMP1 expression as a bona fide aging biomarker for motor neurons. Temporally controlled overexpression of dMMP1 specifically in motor neurons was sufficient to induce deficits in climbing behavior and cause a decrease in neurotransmitter release at neuromuscular synapses. These deficits were reversible if the dMMP1 expression was shut off again immediately after the onset of motor dysfunction. Additionally, repression of dMMP1 enzymatic activity via overexpression of a tissue inhibitor of metalloproteinases delayed the onset of age‐dependent motor dysfunction. MMPs are required for proper tissue architecture during development. Our results support the idea that matrix metalloproteinase 1 is acting as a downstream effector of antagonistic pleiotropy in motor neurons and is necessary for proper development, but deleterious when reactivated at an advanced age. [ABSTRACT FROM AUTHOR]

Life-history theory concerns the trade-offs that mold the patterns of investment by animals between reproduction, growth, and survival. It is widely recognized that physiology plays a role in the mediation of life-history trade-offs, but the details remain obscure. As life-history theory concerns aspects of investment in the soma that influence survival, understanding the physiological basis of life histories is related, but not identical, to understanding the process of aging. One idea from the field of aging that has gained considerable traction in the area of life histories is that life-history trade-offs may be mediated by free radical production and oxidative stress. We outline here developments in this field and summarize a number of important unresolved issues that may guide future research efforts. The issues are as follows. First, different tissues and macromolecular targets of oxidative stress respond differently during reproduction. The functional significance of these changes, however, remains uncertain. Consequently there is a need for studies that link oxidative stress measurements to functional outcomes, such as survival. Second, measurements of oxidative stress are often highly invasive or terminal. Terminal studies of oxidative stress in wild animals, where detailed life-history information is available, cannot generally be performed without compromising the aims of the studies that generated the life-history data. There is a need therefore for novel non-invasive measure- ments of multi-tissue oxidative stress. Third, laboratory studies provide unrivaled opportunities for experimental manipulation but may fail to expose the physiology underpinning life-history effects, because of the benign laboratory environment. Fourth, the idea that oxidative stress might underlie life-history trade-offs does not make specific enough predictions that are amenable to testing. Moreover, there is a paucity of good alternative theoretical models on which contrasting predictions might be based. Fifth, there is an enormous diversity of life-history variation to test the idea that oxidative stress may be a key mediator. So far we have only scratched the surface. Broadening the scope may reveal new strategies linked to the processes of oxidative damage and repair. Finally, understanding the trade-offs in life histories and understanding the process of aging are related but not identical questions. Scientists inhabiting these two spheres of activity seldom collide, yet they have much to learn from each other. [ABSTRACT FROM AUTHOR]