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Activation of the inducible heat shock 71 genes and their role in the heat shock response was studied in vitro in 9.5 day-old rat embryos at neural tube closure. The transcriptional response of a 71 kilodalton (kD) heat shock gene induced after various regimes of heat shock and acquired thermotolerance was investigated. Expression and accumulation of the heat shock (hs) 71 mRNA in the neuroectoderm was studied by Northern and dot blot analysis. Specific expression in various cell types and regions of the neuroectoderm were examined by in situ hybridization. Exposure of embryos to a heat shock at 43 degrees C for 7.5 min caused high levels of hs mRNA 71 accumulation in the neuroectoderm, pronounced protein synthesis inhibition, and regulated recovery. Specific neuroectoderm cell death followed, resulting in major developmental defects of the eye and forebrain region. A mild heat shock of 42 degrees C for 10 min induced the heat shock response, hsp synthesis, and cell recovery, but produced no cell death or deformities. Preheating the embryo at 42 degrees C resulted in acquired thermotolerance to an otherwise teratogenic 43 degrees C heat shock. Thermotolerance was associated with a rapid recovery of protein synthesis associated with hs 71 mRNA expression. Dot blot analysis showed that after a 42 degrees C heat shock, 71 mRNA was rapidly transcribed and transported into the cytoplasm where it was degraded within 2 hr of the initial response. The results suggest that the heat shock protein (hsp) 71 gene may have a protective rather than a rescuing function.

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The prevalence of congenital defects in piglets in a large intensive piggery was determined by autopsy examination of piglets dying in the first week of life and from records kept by the farm staff. A total of 1908 piglets was examined at autopsy and 14,535 were born over the period of the survey. The prevalence of defects on this farm was estimated to be 2.9% of all piglets born, and at least one piglet with a congenital defect was found in 17.4% of litters. Of the piglets dying in the first week 9.5% had a defect and of these 8% had multiple anomalies. The mean litter size at birth for litters with a malformed piglet was 10.9 compared with 9.9 for litters without a malformed piglet. The total preweaning loss in litters containing a malformed pig was higher (29.8%) than that in litters without malformations (17.4%). The antepartum and parturient deaths in litters with a malformed piglet were 35% higher than normal litters. Parturient and anteparturient deaths amounted to 7.5% of piglets born and the total preweaning mortality was 19.9%. Sixty-six per cent of these mortalities occurred within the first week of life. The litter size at birth increased with parity as did the prevalence of litters containing malformed piglets. Neonatal loss was about 2 pigs per litter for all parities. Litter size at birth in litters containing a malformed pig was consistently higher by one pig per litter from all parities, but parturient (7.1%) and anteparturient (1.4%) deaths were also higher in these litters than in litters without malformations (5.1% and 1.2% respectively).(ABSTRACT TRUNCATED AT 250 WORDS)