quently adopted strategies is to interact with additional factors [@pgen.1002688-He2]. YY1 has been shown to directly interact with other ubiquitous factors, Smads, to activate cardiac development genes [@pgen.1002688-Lee1]. Here, we show that YY1 interacts with a lineage-specific transcription factor, M-MITF, to activate critical survival and pigmentation genes in melanocytic cells and that the transcriptional activity of M-MITF is dependent on YY1 for many target genes. Importantly, we demonstrate that despite its ubiquitous expression, YY1 acquires cell type-specific functions by interacting with a lineage-specific transcription factor. Since YY1 most strongly interacts with the intact b-HLH-Zip region of M-MITF ([Figure 3E](#pgen-1002688-g003){ref-type="fig"}), which is present in other non-melanocytic isoforms of MITF, other isoforms of MITF might also interact with YY1 and potentially undergo functional effects within different lineages on the basis of similar biochemical forms of cooperativity. Novel mechanisms through which MITF and YY1 cooperate to confer survival to the melanocyte lineage are interesting subjects for future investigation.

Materials and Methods {#s4}
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Reagents {#s4a}
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Antibodies used were anti-DCT (D-18), anti-YY1 (H-414) and anti-c-Kit (H-300) from Santa Cruz Biotechnology, anti-MITF (C5 mouse monoclonal and rabbit polyclonal) [@pgen.1002688-Du1], anti-Flag (F3165, Sigma) and anti-HA (HA.11, Covance). Anti-Flag M2 agarose beads were obtained from Sigma-Aldrich.

Generation and genotyping of TyrCre, yy1f/f mice {#s4b}
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All animal work has been conducted according to MGH and national guidelines. Male *TyrCre* mouse (Cre transgene is on the X chromosome) [@pgen.1002688-Delmas1] was crossed with *yy1f/f* female mouse to obtain *TyrCre*, *yy1f/+* female (F1). *TyrCre, yy1f/+* F1 female was then crossed with *yy1f/f* male to obtain *TyrCre*, *yy1f/f* male (F2). Genotyping primers are listed in [Table S5](#pgen.10