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S Wampler

Publications and source records attributed to S Wampler.

2 recordsLinked to original sources

Lexicalization in adults who stutter.

Three recent theories have implicated lexical processing failures as a possible source of fluency disruption in persons who stutter. Two experiments that bear upon these theories are reported. Both evaluate the effects on speech response latency of picture naming tasks designed to place selective demands on lexicalization: Experiment I, effects of one-word versus two-word responses; Experiment II, effects of a word's frequency of occurrence versus its number of syllables. Twelve adults who stutter and 12 with normally fluent speech participated in each experiment. In Experiment I, increases in naming latency for two-word (noun + verb) versus one-word (noun or verb) responses showed that demands for parallel processing did not differentiate the experimental groups. However, the between-group difference, showing longer latencies among those who stutter, was six times greater for the verb, than for the noun, task. Moreover, the group difference for verbs fully accounted for the size of the difference in the two-word task. Experiment II showed that the relative increase in naming latency associated with the word frequency effect versus the syllable latency effect was significantly greater in the stuttering than the nonstuttering group. Outcomes of the two experiments suggest that during lexicalization, as early as the L1 stage and first phase of L2, slow processing could serve to disrupt fluency in some persons who stutter. Under certain conditions, as specified in the three theories cited, such disruptions could set the occasion for stutter events.

Adult↗

Interaction between a transcriptional activator and transcription factor IIB in vivo.

Transcription of messenger RNA-encoding genes in vitro requires many protein factors. Transcription factor IID, possibly with the cooperation of TFIIA, binds to the TATA element of the promoter, forming a complex that can bind TFIIB (refs 6, 7) followed by RNA polymerase II (refs 6, 8) and other factors. One or more of these steps is thought to be facilitated by gene-specific transcriptional activation proteins; this seems to require TFIID-associated auxiliary factors and may involve direct contact between the activator and TFIID and/or TFIIB. If such contact is necessary in vivo, activation might conceivably be blocked by a TFIIB derivative containing the sequences necessary for this interaction, but lacking those necessary for binding to the rest of the transcriptional apparatus, an effect similar to that referred to as squelching or transcriptional interference. Here we show that the activity of the glutamine-rich fushi tarazu activation domain is indeed blocked by truncated TFIIB derivatives in Drosophila Schneider L2 cells, suggesting that it is mediated by interactions with TFIIB.

Animals↗