Sex differences in the electrocommunication signals of the electric fish Apteronotus bonapartii

The South American weakly-electric knifefish (Apteronotidae) produce highly diverse and readily quantifiable electrocommunication signals. The electric organ discharge frequency (EODf), and EOD modulations (chirps and gradual frequency rises (GFRs)), vary dramatically across sexes and species, presenting an ideal opportunity to examine the proximate and ultimate bases of sexually dimorphic behavior. We complemented previous studies on the sexual dimorphism of apteronotid communication signals by investigating electric signal features and their hormonal correlates in Apteronotus bonapartii, a species which exhibits strong sexual dimorphism in snout morphology. Electrocommunication signals were evoked and recorded using a playback paradigm, and were analyzed for signal features including EOD frequency and the structure of EOD modulations. To investigate the androgenic correlates of sexually dimorphic EOD signals, we measured plasma concentrations of testosterone and 11-ketotestosterone. A. bonapartii responded robustly to stimulus playbacks. EODf was sexually monomorphic, and males and females produced chirps with similar durations and amounts of frequency modulation. However, males were more likely than females to produce chirps with multiple frequency peaks. Sexual dimorphism in apteronotid electrocommunication signals appears to be highly evolutionarily labile. Extensive interspecific variation in the magnitude and direction of sex differences in EODf and in different aspects of chirp structure suggest that chirp signals may be an important locus of evolutionary change within the clade. The weakly-electric fish represent a rich source of data for understanding the selective pressures that shape, and the neuroendocrine mechanisms that underlie, diversity in the sexual dimorphism of behavior.     

分裂中期的CHO细胞能对其染色体DNA进行切除修补吗?

以中国仓鼠细胞CHO-K_1为材料,用放射自显术检查紫外线照射后细胞内DNA的切除修补,没有得到足以证明分裂中期细胞对其染色体DNA进行切除修补的可靠证据。此结果与1977年Ikushima所报告的不同。对于这种修补能力的缺乏,作者认为应考虑到的原因至少有:(1)分裂中期染色体上的DNA处在高度紧密的状态,难于进行切除修补;(2)分裂中期细胞中担任DNA修补合成的多聚酶β的活性可能下降;(3)分裂中期细胞的核膜解体。