We also noted that these genes show an identical increase in expr

We also noted that these genes show an identical increase in expression in the GluRIIA mutant. Since the ppk11 and ppk16 genes are separated

by only 63 base pairs, we considered the possibility that these genes might be cotranscribed. To test this idea, we generated PCR primers that could specifically amplify either full-length ppk11, ppk16, or both genes together as part of a single transcript. We Gemcitabine concentration find that we are able to isolate full-length cDNAs for ppk11, ppk16, and a cDNA that spans the coding regions of both ppk11 and ppk16 and is of the expected size for a transcript containing both ppk11 and ppk16 ( Figure 6D). The identity of the joint ppk11-ppk16 transcript was confirmed by sequencing the junction between the ppk11 and ppk16 genes. A stop codon is present in the joint cDNA following the ppk11 coding sequence, suggesting that the two genes are cotranscribed and translated as independent proteins. This result is reproducible across three independently derived cDNA libraries (data not shown). These data indicate that ppk11 and ppk16 are cotranscribed and coregulated during synaptic homeostasis,

further suggesting that they could be subunits of a single channel that is upregulated during the sustained expression of synaptic homeostasis. We next asked whether ppk11 and ppk16 are not only cotranscribed and coregulated during synaptic homeostasis, but whether they function as part of a single genetic unit during synaptic homeostasis. If two genes function as part of a single genetic unit, then disrupting the expression of one gene will also affect the Cabozantinib in vivo other gene. To test this,

we performed a series of complementation experiments, diagrammed in Figure 6F. First, we show that heterozygous mutations in either the ppk11 (+,ppk11PBac/+,+) or the ppk16 genes (ppk16Mi,+/+,+) do not alter synaptic homeostasis ( Figures 6E and 6F). Next, we demonstrate that a heterozygous deficiency that encompasses both ppk11 and ppk16 (ppk16Df,ppk11Df/+,+) also does not alter synaptic homeostasis ( Figures 6E and 6F). Therefore, animals that harbor one functional copy of ppk11 and one functional copy of ppk16 can express normal synaptic homeostasis. However, when the heterozygous +,ppk11Pbac/+,+ many mutation is placed in trans to the heterozygous ppk16Mi,+/+,+ mutation (+,ppk11PBac/ ppk16Mi,+), then we find that synaptic homeostasis is completely blocked ( Figures 6E and 6F). Although each mutation is heterozygous, they are resident on different chromosomes. As such, the heterozygous mutation in ppk11 could disrupt the remaining functional copy of ppk16 and vice versa ( Figure 6F). Since homeostasis is blocked when heterozygous mutations are placed in trans but not when they are placed in cis, we conclude that one or both of the mutations must affect both ppk11 and ppk16.

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