Monitoring changes in back fat thickness and its effect on the restoration of ovarian activity and fertility in Bos indicus cows

With the objective of testing the hypothesis if animals with a stable layer of body fat (FAT) during the peripartum have a better chance of becoming pregnant after calving, fifty‐nine multiparous Brahman cows in their last trimester of pregnancy were used. Animals averaged four parturitions and were stocked at a rate of 1.25 animal units per hectare and divided into two groups depending on the time postpartum (dpp) that the intravaginal releasing device CIDR was inserted; Group 1 (<30 dpp; n = 30) received the implant at 25.2 ± 4.21 and withdrawn 9 days later. Group 2 (≥30 dpp; n = 29) received the CIDR at 38.41 ± 5.8. Animals were AI at detected oestrus until 170 dpp and calculated as pregnant at first service or requiring more than one service (1s and >1s), not pregnant but cycling (not pregnant) and those not cycling at all (anestrus). The FAT measurements were taken twice each month from the last trimester of gestation until 96 dpp. The onset of ovarian activity was monitored through blood levels of progesterone (P4) at days 14 and 9 prior to CIDR insertion and days 10, 13, 30 and 33 after CIDR withdrawal. Animals pregnant did not have any major changes in their fat thickness. In contrast, cows pregnant in the group ≥30 dpp had changes in their FAT homoeostasis, and pregnant animals in the 1s and >1s groups did not show differences in dorsal back fat in the last trimester of pregnancy and early postpartum. In contrast, animals not pregnant and in anestrus FAT values decreased considerably after parturition. Overall, fertility was 49%, but 18% of all the animals remained anestrus losing FAT. Thus, animals with adequate metabolic conditions will have a better chance of pregnancy regardless of the time postpartum when the reproductive programme starts.     

Compensated deleterious mutations in insect genomes

Relatively little is known about the importance of amino acid interactions in protein and phenotypic evolution. Here we examine whether mutations that are pathogenic in Drosophila melanogaster become fixed via epistasis in other Dipteran genomes. Overall divergence at pathogenic amino acid sites is reduced. However, approximately 10% of the substitutions at these sites carry the exact same pathogenic amino acid found in D. melanogaster mutants. Hence compensatory mutation(s) must have evolved. Surprisingly, the fraction 10% is not affected by phylogenetic distance. These results support a selection-driven process that allows compensated amino acid substitutions to become rapidly fixed in taxa with large populations.