Leaf senescence can impact crop production by either changing photosynthesis duration, or by modifying the nutrient remobilization efficiency and harvest index. The doubling of the grain yield in major cereals in the last 50 years was primarily achieved through the extension of photosynthesis duration and the increase in crop biomass partitioning, two things that are intrinsically coupled with leaf senescence. In this review, we consider the functionality of a leaf as a function of leaf age, and divide a leaf's life into three phases: the functionality increasing phase at the early growth stage, the full functionality phase, and the senescence and functionality decreasing phase. A genetic framework is proposed to describe gene actions at various checkpoints to regulate leaf development and senescence. Four categories of genes contribute to crop production: those which regulate (I) the speed and transition of early leaf growth, (II) photosynthesis rate, (III) the onset and (IV) the progression of leaf senescence. Current advances in isolating and characterizing senescence regulatory genes are discussed in the leaf aging and crop production context. We argue that the breeding of crops with leaf senescence ideotypes should be an essential part of further crop genetic improvement.Keywords: Leaf Senescence; photosynthesis and photoassimilates; nutrient remobilisation; senescence-associated genes; crop ideotypes.

T cells have a crucial role in viral clearance and vaccine response; however, the mechanisms regulating their responses to viral infections or vaccinations remain elusive. In this study, we investigated T-cell homeostasis, apoptosis, DNA damage, and repair machineries in a large cohort of subjects with hepatitis C virus (HCV) infection. We found that naive CD4 T cells in chronically HCV-infected individuals (HCV T cells) were significantly reduced compared with age-matched healthy subjects. In addition, HCV T cells were prone to apoptosis and DNA damage, as evidenced by increased 8-oxoguanine expression and γH2AX/53BP1-formed DNA damage foci—hallmarks of DNA damage responses. Mechanistically, the activation of DNA repair enzyme ataxia telangiectasia mutated (ATM) was dampened in HCV T cells. ATM activation was also diminished in healthy T cells exposed to ATM inhibitor or to HCV (core protein) that inhibits the phosphoinositide 3 kinase pathway, mimicking the biological effects in HCV T cells. Importantly, ectopic expression of ATM was sufficient to repair the DNA damage, survival deficit, and cell dysfunctions in HCV T cells. Our results demonstrate that insufficient DNA repair enzyme ATM leads to increased DNA damage and renders HCV T cells prone to apoptotic death, which contribute to the loss of naive T cells in HCV infection. Our study reveals a novel mechanism for T-cell dysregulation and viral persistence, providing a new strategy to improve immunotherapy and vaccine responses against human viral diseases.

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