Background Information:

In the nervous system, the brain processes information bytransmission of electrical and chemical signals through a networkof neurons. These signals travel through synapses which connect twoneurons. Neuroligins are cell-adhesion molecules that function toconnect two neurons at synapses and mediate proper signallingacross the synapse. Interestingly, neuroligin function has beenlinked to autism spectrum disorder (ASD) which is primarilymanifested by delayed development and deficiency in socialinteraction and communication in patients. Mutations in genesencoding neuroligins have been identified in ASD patients. Themolecular mechanism of how neuroligins function in ASD has beeninvestigated using mouse models. The mouse gene NL3encodes a neurolignin. Aberrant NL3 gene function in miceresults in synaptic dysfunction and a diverse range of abnormalbehavior including a subset that resembles ASD patients. A strikingphenotype of NL3 mutant mice is increased repetitivebehavior compared to wild type/normal mice.

There are two alleles of the mouse NL3gene. One allele (referred as “+” or wildtype) produces NL3 protein which results in the synthesisof neuroligins for synaptic function. In contrast, the other allele(referred as “-”) does not produce anyNL3 mRNA (and hence no NL3 protein) resulting in aninability to produce neuroligins.

Question: Closer examination of the two alleles of the mouseNL3 gene reveals no changes in nucleotide sequence in thetranscriptional unit. This observation indicates that thedifference in nucleotide sequence between the two alleles must notoccur within the transcriptional unit. Provide two possibilitieswhere nucleotide changes could occur on the chromosome forthe allele that does not produce any NL3 mRNA and explainwhy.