For instance, UNC5 homologs are highly expressed in developing limbs. Similarly, FA genes are expressed primarily in cells of mesenchymal origin that give rise to forelimb and hind limb tissues. Consequently, defective FA genes result in limb malformations, and patients with FA can show absence or underdevelopment of thumbs and short or hypoplastic radii. In view of our results that FANCC negatively impacts UNC5A’s ability to induce apoptosis, we propose that dysregulation of UNC5A’s apoptotic signal could lead to developmental defects similar to those observed in FA patients. It is well known that FANCC suppresses apoptosis; FANCCdepleted cells or patient-derived cells with FANCC mutations show increased LEE011 apoptosis induced by various cellular stressors, such as DNA damage, inhibitory cytokines, and oxygen radicals, whereas FANCC over-expression delays onset of apoptosis. FANCC is also regulated by caspase-mediated cleavage, which inactivates its ability to suppress apoptosis. The fact that FANCC directly interacts with the UNC5A C-terminal end harboring the DD suggests that interaction of both proteins may interfere with death signal transmission. It has been proposed that UNC5A mediates apoptosis via its C-terminal DD, although conflicting data suggest that the ZU-5 C-terminal domain, which binds the melanoma antigen gene D1, is required for apoptosis. The UNC5A homolog protein UNC5B was shown to directly interact with the death-associated protein kinase via its DD. This UNC5B/DAPK interaction was shown to be required for activation of the apoptotic cascade. Although UNC5A did not directly bind DAPK, regulation of DAPK activation via protein phosphatase 2A was shown to be required for UNC5A-mediated apoptosis. We identified a direct interaction between FANCC and the C-terminal region of UNC5A, including the ZU-5 and DD, suggesting that FANCC binding with UNC5A may interfere with UNC5A binding to apoptosis-promoting factors, such as MAGED1. Consequently, FANCC may act as a cellular sensor of UNC5A-mediated apoptotic cues and prevent or delay apoptosis depending on the tissue or cellular context. Periodic advances in DNA sequencing technology, such as wide-spread adoption of automated DNA sequencing in the 1990s, have revolutionized understanding of microbial processes, from single-cell physiology to population biology. The last decade saw the increased use of high-throughput or ‘next-generation’ sequencing methods that parallelize the DNA sequencing process beyond what was possible with standard dye-terminator methods. These technologies have underpinned important research in pathogen epidemiology and evolution, but there are still major technical challenges for effectively archiving and analyzing hundreds or thousands of bacterial genomes. A popular approach to describe the genetic variation among multiple bacterial genomes has been to map stretches of DNA sequences from multiple isolates to a reference bacterial genome to identify variable sites that display single nucleotide polymorphisms.