High impact information on slp2

• We propose that by virtue of their ability to activate wg and repress en expression, the distribution of the slp proteins define the wg-competent and en-competent groups [1].
• Removal of slp gene function causes embryos to exhibit a severe pair-rule/segment polarity phenotype [1].
• The phenotypes of embryos containing various combinations of functional slp genes suggest that for early slp function, until gastrulation, only slp1 is required [2].
• Low levels of terminal system activity seem to potentiate bcd as an activator of slp, whereas high levels down-regulate bcd rendering it inactive [3].
• In Tribolium, homologs of almost all the eight canonical Drosophila pair-rule genes are expressed in pair-rule domains, but only five have pair-rule functions. even-skipped, runt and odd-skipped act as primary pair-rule genes, while the functions of paired (prd) and sloppy-paired (slp) are secondary [4].

Biological context of slp2

• In contrast, misexpression of either slp1 or slp2 causes downregulation of glial cell-specific genes and alters the fate of glial and neuronal cells [5].

Anatomical context of slp2

• The sloppy-paired (slp) locus contains two genes (slp1 and slp2) that are expressed in overlapping striped patterns in the presumptive thorax and abdomen [6].

Regulatory relationships of slp2

• Similarly, slp is required to activate wg in alternate parasegments and to maintain the remaining wg stripes in both insects [4].

Other interactions of slp2

• In this paper, we also show that gsb interacts with slp and prevents Slp from specifying NB4-2 identity [7].
• We also propose that in wg-expressing ectodermal cells, slp is an integral component in an autocrine feedback loop of Wg signaling [8].

References