<p dir="ltr">Uncovering the mechanisms of senescence in maize will give us a deeper understanding needed to drive future yield increases. Previous work on senescence response to sink disruption has identified a set of genes and biochemical mechanisms. Still, little is understood about the impact of this phenotype on yield and other commercially relevant traits. Uncovering the genetic basis of senescence in maize and testing the effect of these alleles on yield will provide a mechanistic framework for considering this trait to drive future yield increases.</p><p dir="ltr">Ear removal experiments demonstrated that senescence timing is insensitive to the presence or absence of an ear outside a critical window from 10 to 45 days after pollination. Nitrogen fertilization did not impact the SSRS response measured in the upper canopy. In further characterizing the SSRS phenotype, we have provided a spatial and temporal map of the B73 senescence response to sink disruption from the top of the plant to the ear leaf and discovered that this phenomenon is dose dependent and proportional to the size of the sink across two genotypes and years. This relationship was successfully used to predict kernel numbers and grain weight from spectral leaf properties as early as 4 weeks after pollination using remote sensing under agronomic conditions.</p><p dir="ltr">A population of 343 exPVP inbred lines was evaluated for source-sink regulated senescence and hybrid testcrosses were made for a subset of 200 inbred lines to testers for measurement of yield and ear photometry phenotypes. Source-sink regulated senescence of inbred parents was correlated with the yield of intra-family hybrids but was not generally correlated with the yield of hybrids made from crosses between two heterotic groups. The presence of multiple significant SNP association at the Bonferroni-corrected threshold at loci that are associated both with kernel traits and SSRS suggests shared genetic regulation of two traits that is likely driving the observed trait correlations of SSRS with kernel size and yield.</p><p dir="ltr">The maize nested association mapping (NAM) parents reveal a previously unknown breadth of SSRS phenotypes in the global diversity of maize germplasm. Mapping genes for SSRS in the NAM populations supports previously reported loci with large, dominant effects as well as evidence for previously unreported modifiers that are capable of suppressing the dominant alleles and producing a quantitative distribution in SSRS phenotypes. There are distinct alleles within sub-populations worth further study such as sweetcorn populations with non-senescence responses to sink disruption. A multi-factor analysis for QTL mapping, GWAS, and mutant variant sequencing identified highly significant loci on chromosomes 1 from 30.4Mbp to 35.8Mbp, chromosome 2 from 183.2Mbp to 190.8Mbp, chromosome 4 from 38.2Mbp to 134.8Mbp (crosses a centromere), chromosome 5 from 140.8Mbp to 233.9Mbp, chromosome 8 from 112.5Mbp to 123.8Mbp, and chromosome 8 from 155.7Mbp to 163.9Mbp. Candidate genes co-located with Bonferroni SNP in these regions may contribute to SSRS phenotypes through regulation of autophagy, accumulation of flavonoids, and sequestration of sugar in cell walls as an alternative sink. It is possible that co-regulation of these genes could cause all of them to be involved in the stress response of B73 to sugar accumulation. To find the causal variants for these traits, fine mapping and comparisons of near-isogenic lines will be required to narrow the list of candidate genes. Uncovering the alleles responsible for SSRS in global maize diversity could provide the building blocks for a physiological approach to increasing yields through optimizing the senescence responses to elevated sugar levels during grain-fill.</p>