Question

Growth in nutrient-rich medium represses expression of the yeast serine biosynthesis gene SER3. Martens et al. repressed SER3 expression and found a highly transcribed region of DNA upstream of the SER3 gene. This upstream region contains a non-protein-coding gene called SRG1. An RNA polymerase binds the SRG1 promoter and transcribes the SRG1 gene through the adjacent SER3 promoter, which leads to the repression of SER3. Mutations in the SRG1 promoter remove the repression of SER3. Which of the following statements explains how SRG1 transcription represses SER3 transcription?

1) Transcription machinery on the SRG1 gene prevents binding of transcription factors on the SER3 promoter, blocking SER3 transcription.
2) The protein product of the SRG1 gene binds to the SER3 promoter and prevents its transcription.
3) SRG1 RNA modifies the histones in the region of the SER3 promoter, creating a heterochromatic region around the SER3 gene.
4) The SRG1 transcription process occurs at such a high rate that it titrates basal transcription factors away from other initiation sites.

Answer 1

The repression of SER3 transcription by SRG1 is due to the interference of SRG1 transcription machinery with the SER3 promoter, preventing transcription factors from initiating SER3 transcription.

Step-by-step explanation:

In the case of the yeast SER3 gene regulation, the repression of SER3 transcription is due to the transcriptional activity at the non-protein-coding gene SRG1. When RNA polymerase binds to the SRG1 promoter and transcribes SRG1, it overlaps with the adjacent SER3 promoter. This overlapping transcription likely hinders the binding of transcription machinery on the SER3 promoter, thereby blocking transcription factors from accessing SER3’s regulatory sequences and initiating its transcription. This phenomenon is described in statement 1), where transcription machinery on the SRG1 gene prevents binding of transcription factors on the SER3 promoter, which blocks SER3 transcription. Mutations in the SRG1 promoter that remove this repression, resulting in the activation of SER3 transcription, further support this mechanism.