Perceptual Compensation Is Correlated with Individuals' “Autistic” Traits: Implications for Models of Sound Change

Variation is a ubiquitous feature of speech. Listeners must take into account context-induced variation to recover the interlocutor''s intended message. When listeners fail to normalize for context-induced variation properly, deviant percepts become seeds for new perceptual and production norms. In question is how deviant percepts accumulate in a systematic fashion to give rise to sound change (i.e., new pronunciation norms) within a given speech community. The present study investigated subjects'' classification of /s/ and // before /a/ or /u/ spoken by a male or a female voice. Building on modern cognitive theories of autism-spectrum condition, which see variation in autism-spectrum condition in terms of individual differences in cognitive processing style, we established a significant correlation between individuals'' normalization for phonetic context (i.e., whether the following vowel is /a/ or /u/) and talker voice variation (i.e., whether the talker is male or female) in speech and their “autistic” traits, as measured by the Autism Spectrum Quotient (AQ). In particular, our mixed-effect logistic regression models show that women with low AQ (i.e., the least “autistic”) do not normalize for phonetic coarticulation as much as men and high AQ women. This study provides first direct evidence that variability in human''s ability to compensate for context-induced variations in speech perceptually is governed by the individual''s sex and cognitive processing style. These findings lend support to the hypothesis that the systematic infusion of new linguistic variants (i.e., the deviant percepts) originate from a sub-segment of the speech community that consistently under-compensates for contextual variation in speech.     

Biosynthesis of man-β-G1cNAc-G1cNAc-pyrophosphoryl-polyprenol by a solubilized enzyme from aorta

The particulate enzyme fraction from pig aorta was treated with Triton X-100 or Nonidet P-40 to yield a soluble enzyme preparation. This solubilized enzyme catalyzed the transfer of mannose from GDP-[¹⁴C]mannose, but not from [¹⁴C]mannosyl-phosphoryl-polyprenol, to G1cNAc-G1cNAc-pyrophosphoryl-polyprenol to form the trisaccharide-lipid, Man-β-GlcNAc-GlcNAc-pyrophosphoryl-polyprenol. The trisaccharide-lipid formed in these reactions was isolated by solvent fractionation and was subjected to mild acid hydrolysis to release the [¹⁴C]trisaccharide. Essentially all of the radioactivity was released from this trisaccharide as mannose upon treatment with β-mannosidase while α-mannosidase had no effect.     

Oxidation-reduction potential dependence of low-temperature photoreactions of chloroplast Photosystem II

The light-induced free-radical signal of Photosystem II (observed after illumination at 77 °K) has been studied in chloroplasts as a function of the oxidation-reduction potential established prior to freezing. The intensity of the light-induced signal is unchanged in the potential region of +590 mV to +760 mV. At higher potential (+850 mV), there is a 30% decrease in signal intensity. The light-induced signal decreases to zero in the low-potential region, with a midpoint potential of +475 mV. These results are considered in terms of a Photosystem II reaction-center complex in which the light-induced free-radical signal arises from the oxidized form of the reaction-center chlorophyll, and this chlorophyll molecule is capable of being reduced at liquid-nitrogen temperature by a secondary electron donor which has a midpoint oxidation-reduction potential of +475 mV.     

Structural and functional variability among DQ β alleles of DR2 subtypes

Homozygous lymphoblastoid cell lines representing various Dw subtypes of DR2 were examined for polymorphism at the DQ locus by molecular and cellular techniques. The subtypes studied included Dw2, Dw12, and a group heterogenous by cellular typing that we shall refer to as non-Dw2/non-Dw12. Restriction fragment length polymorphism analysis of cell lines representing these subtypes revealed DQ -specific patterns consistent with cellular typing. Two-dimensional gel electrophoresis of DQ molecules from representative cell lines revealed a structural polymorphism of DQ among the three subtypes. The DQ chain migrated to a position that was unique to each subtype and was consistent among various representative cell lines of each subtype. Nucleotide sequence analysis of cDNA clones of DQ from Dw2, Dw12, and non-Dw2/non-Dw12 lines confirmed that the variability resided at the genetic level. Variability was found in the form of numerous scattered nucleotide substitutions throughout the first domain of these alleles. The DQ gene of the non-Dw2/non-Dw12 cell line AZH was further found to be almost identical with the DQ gene of a DR1 line (Bell et al. 1985b), implicating a common evolutionary origin of these alleles. The only difference between these two sequences was due to an apparent gene conversion event at amino acid 57. T-cell cloning experiments resulted in the derivation of Epstein-Barr virus-specific, DQw1-restricted clones that proliferated against only those cell lines that exhibited the DQ gene common to AZH and the DR1 cell line. Thus, the polymorphism among DQ alleles within DR2 results in subtype-specific restriction.