These screens take advantage of a novel aspect of yeast repair biology. Yeast have a compact, non-redundant genome with few repeated genes or repetitive DNA sequences. This promotes IR-induced DSB damage to be preferentially repaired by homologous recombination which requires an undamaged homolog or sister chromatid to template a successful repair event. Haploid yeast cells lack a homolog in G1 or early S phase, where sister chromatids may only be partially replicated. Therefore, in unsynchronized haploid cells that have been irradiated throughout the cell cycle, as radiation dose increases, a rapid dose-dependent decline in survival is observed followed by a more gradual radioresistant decline in survival. This two-component survival response has been attributed to the exquisite radiosensitivity of haploid cells in G1 where no homolog is available to template a successful recombinational repair event. Under these circumstances in G1 cells, one DSB ”hit” is lethal. Malignant melanoma is capable of rapid progression and the prognosis of the advanced stages of the disease is extremely poor. Angiogenesis represents an essential step in its multistage progression and antiangiogenic agents are currently tested in patients with advanced melanoma. A vital role in tumor angiogenesis is played by the Vascular Endothelial Growth Factor, but the associated expression of both VEGF and its receptors by most advanced stage melanomas also suggests the possibility of an autocrine loop within the melanoma cells. This is supported by the demonstrated ability of VEGF to stimulate proliferation and migration of these cells. Although two VEGF receptors are known, VEGF-R1/flt-1 and VEGFR-2/KDR/flk-1, VEGF was shown to signal mainly through VEGFR-2, which upon ligand binding becomes tyrosine phosphorylated and activates multiple signaling networks. In accordance with this, patients with high VEGFR-2 expression in melanoma lesions were shown to be more likely to respond to Sorafenib WZ8040 therapy, a multitarget kinase inhibitor. This is likely due to inhibition of both angiogenesis and cell proliferation driven by the presence of a VEGF/VEGFR-2 autocrine loop in tumor cells. The second, radio-resistant repair component is thought to reflect the capability of cells in late S and G2 phases to repair IR-induced DSBs by recombination. Since diploid mutants have a chromosome homolog in G1, they are radioresistant throughout the cell cycle and thus facilitate the detection of previously unknown DSB repair gene mutants that impact checkpoint and/or recombinational repair functions in G1 or early S phase prior to the completion of DNA synthesis. In contrast to the changes observed in the number of GLR-1 punctae during repeated longterm mechano-stimulation, we found that associative learning regulates the average size but not the number of GLR-1 positive synapses.