Hendrickson J E, Sakonju S
Department of Human Genetics, Howard Hughes Medical Institute, University of Utah, Salt Lake City 84112, USA.
Genetics. 1995 Feb;139(2):835-48. doi: 10.1093/genetics/139.2.835.
The infra-abdominal (iab) elements in the bithorax complex of Drosophila melanogaster regulate the transcription of the homeotic genes abdominal-A (abd-A) and Abdominal-B (Abd-B) in cis. Here we describe two unusual aspects of regulation by the iab elements, revealed by an analysis of an unexpected complementation between mutations in the Abd-B transcription unit and these regulatory regions. First, we find that iab-6 and iab-7 can regulate Abd-B in trans. This iab trans regulation is insensitive to chromosomal rearrangements that disrupt transvection effects at the nearby Ubx locus. In addition, we show that a transposed Abd-B transcription unit and promoter on the Y chromosome can be activated by iab elements located on the third chromosome. These results suggest that the iab regions can regulate their target promoter located at a distant site in the genome in a manner that is much less dependent on homologue pairing than other transvection effects. The iab regulatory regions may have a very strong affinity for the target promoter, allowing them to interact with each other despite the inhibitory effects of chromosomal rearrangements. Second, by generating abd-A mutations on rearrangement chromosomes that break in the iab-7 region, we show that these breaks induce the iab elements to switch their target promoter from Abd-B to abd-A. These two unusual aspects of iab regulation are related by the iab-7 breakpoint chromosomes that prevent iab elements from acting on Abd-B and allow them to act on abd-A. We propose that the iab-7 breaks prevent both iab trans regulation and target specificity by disrupting a mechanism that targets the iab regions to the Abd-B promoter.
果蝇黑腹果蝇双胸复合体中的腹下(iab)元件顺式调控同源异型基因腹部-A(abd-A)和腹部-B(Abd-B)的转录。在此,我们描述了iab元件调控的两个不同寻常的方面,这是通过对Abd-B转录单元与这些调控区域的突变之间意外互补的分析揭示的。首先,我们发现iab-6和iab-7可以反式调控Abd-B。这种iab反式调控对破坏附近Ubx位点转座效应的染色体重排不敏感。此外,我们表明位于Y染色体上的一个转座的Abd-B转录单元和启动子可以被位于第三条染色体上的iab元件激活。这些结果表明,iab区域能够以一种比其他转座效应更不依赖同源配对的方式调控位于基因组远处位点的靶启动子。iab调控区域可能对靶启动子具有非常强的亲和力,使得它们尽管受到染色体重排的抑制作用仍能相互作用。其次,通过在iab-7区域断裂的重排染色体上产生abd-A突变,我们表明这些断裂会诱导iab元件将其靶启动子从Abd-B切换到abd-A。iab调控的这两个不同寻常的方面通过iab-7断点染色体联系起来,这些染色体阻止iab元件作用于Abd-B并使其能够作用于abd-A。我们提出,iab-7断裂通过破坏一种将iab区域靶向Abd-B启动子的机制,阻止了iab反式调控和靶特异性。