High impact information on mip130

• Surprisingly, Dm-myb mip130 double mutants are also viable and display the same phenotypes as mip130 mutants alone [1].
• Dm-myb mutant lethality in Drosophila is dependent upon mip130: positive and negative regulation of DNA replication [1].
• We found that mip130 mutant females are sterile and display inappropriate bromodeoxyuridine (BrdU) incorporation throughout the follicle cell nuclei at stages undergoing gene amplification [1].
• Together, these data support a model in which DmMyb activates a repressive complex containing Mip130 into a complex competent to support replication at specific loci in a temporally and developmentally proscribed manner [1].
• Members of the novel family of proteins that include Drosophila Mip130, Caenorhabditis elegans LIN-9, and mammalian LIN-9 intervene in different cellular functions such as regulation of transcription, differentiation, transformation, and cell cycle progression [2].

Other interactions of mip130

• This suggests that Mip130 activity without DmMyb counteraction may be responsible for the Dm-myb mutant lethality [1].

References