Developmental timing scales wing patterning between avian species

How development is timed between differently sized species is a fundamental question in biology. To address this problem, we compared wing development in the quail and the larger chick. We reveal that developmental timing is faster in the quail than in the chick, and is associated with pattern specification, proliferation, organiser duration, differentiation and apoptosis. However, developmental timing is independent of the growth rate, which is equivalent between both species, and therefore scales pattern to the size of the wing. We reveal that developmental timing can be either maintained or reset in interspecies tissue grafts, and we implicate retinoic acid as the resetting signal. Accordingly, retinoic acid can switch species developmental timing and rescale pattern, both between the quail and chick, and the chick and the larger turkey. We suggest that the scaling of pattern to wing bud size is achieved by the modulation of developmental timing against a comparable rate of growth.Summary- We show that developmental timing scales wing patterning

GFAT and PFK genes show contrasting regulation of chitin metabolism in Nilaparvata lugens

Glutamine:fructose-6-phosphate aminotransferase (GFAT) and phosphofructokinase (PFK) are enzymes related to chitin metabolism. RNA interference (RNAi) technology was used to explore the role of these two enzyme genes in chitin metabolism. In this study, we found that GFAT and PFK were highly expressed in the wing bud of Nilaparvata lugens and were increased significantly during molting. RNAi of GFAT and PFK both caused severe malformation rates and mortality rates in N. lugens. GFAT inhibition also downregulated GFAT, GNPNA, PGM1, PGM2, UAP, CHS1, CHS1a, CHS1b, Cht1-10, and ENGase. PFK inhibition significantly downregulated GFAT; upregulated GNPNA, PGM2, UAP, Cht2-4, Cht6-7 at 48 h and then downregulated them at 72 h; upregulated Cht5, Cht8, Cht10, and ENGase; downregulated Cht9 at 48 h and then upregulated it at 72 h; and upregulated CHS1, CHS1a, and CHS1b. In conclusion, GFAT and PFK regulated chitin degradation and remodeling by regulating the expression of genes related to the chitin metabolism and exert opposite effects on these genes. These results may be beneficial to develop new chitin synthesis inhibitors for pest control.

An autoregulatory cell cycle timer integrates growth and specification in chick wing digit development

A fundamental question is how proliferation and growth are timed during embryogenesis. Although it has been suggested that the cell cycle could be a timer, the underlying mechanisms remain elusive. Here we describe a cell cycle timer that operates in Sonic hedgehog (Shh)-expressing polarising region cells of the chick wing bud. Our data are consistent with Shh signalling stimulating polarising region cell proliferation via Cyclin D2, and then inhibiting proliferation via a Bmp2-p27kip1 pathway. When Shh signalling is blocked, polarising region cells over-proliferate and form an additional digit, which can be prevented by applying Bmp2 or by inhibiting D cyclin activity. In addition, Bmp2 also restores posterior digit identity in the absence of Shh signalling, thus indicating that it specifies antero-posterior (thumb to little finger) positional values. Our results reveal how an autoregulatory cell cycle timer integrates growth and specification and are widely applicable to many tissues.

A positional information gradient of sonic hedgehog is required for flight feather formation in avian wings

Flight is a triumph of evolution that enabled the radiation and success of birds. A crucial step was the development of forelimb flight feathers that may have evolved for courtship or territorial displays in ancestral theropod dinosaurs. Classical tissue recombination experiments performed in the chick embryo provide evidence that signals operating during early limb development specify the position and identity of feathers. Here we show that a positional information gradient of Sonic hedgehog (Shh) signalling in the embryonic chick wing bud specifies the pattern of adult flight feathers in a defined spatial and temporal sequence that reflects their different identities. We reveal that the Shh signalling gradient is interpreted into specific patterns of flight feather-associated gene expression. Our data suggests that flight feather evolution involved the co-option of the pre-existing digit patterning mechanism and therefore uncovers an embryonic process that played a fundamental step in the evolution of avian flight.