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Mycobacteroides abscessus (MAB) is an opportunistic infection that predominately causes respiratory infections particularly in patients with underlying lung abnormalities, as well as skin infections. MAB can display two different colony morphotypes: smooth (MABS) and rough (MABR). In the clinic, the MAB morphotype is not routinely recorded nor is the colonizing morphotype considered for choosing the treatment plan. This is particularly worrying because case reports indicate that the transition to the rough morphotype causes decreased lung function and increased mortality. Several groups have shown that genetically matched morphotypes differ in survival when exposed to antibiotics, an anoxic environment, sera, and reactive oxygen species. Although the differences between the two morphotypes may be due to the difference in GPL expression on the surface of MABS, bacteria morphology not only contributes to surface changes but also has broad reaching physiological changes for several pathogens such as Pseudomonas aeruginosa, Mycobacterium smegmatis, Vibrio cholera, and Bacillus subtills. To provide a molecular understanding of why MABS and MABR are phenotypically distinct, we generated transposon insertion libraries in both morphotypes. We found that while they share 441 essential genes, MABS has 165 unique essential genes and MABR has 65. We have also developed a murine abscess model which will serve as a model to further examine morphotype specific gene essentiality during infection.