RESUMEN
Pollination is the primary step in seed formation. Pollination biologists have shown that pollination failure can occur at all steps in the dispersal process and at several different levels. Increased risk of pollination failure is associated with pollen if it is delivered to a stigma too little, too much, too late, too mixed in composition or too poor in quality. It is associated with pollinators when they are too few or too inconstant, and with plants when they are too specialized or too selective. It is associated with populations when they are too sparse, too small in number or too uniform genetically, and with communities when they are too fragmented, genetically impoverished or under rapid modification. Understanding the causes of pollination failure in plants can aid the successful conservation and recovery of rare plants, maintenance of crop yields, and sustainable use of wild plant resources such as forest timber.
Asunto(s)
Fenómenos Fisiológicos de las Plantas , Polen/fisiología , Agricultura , Animales , Conservación de los Recursos Naturales , Ambiente , Insectos/fisiología , Tallos de la Planta/fisiología , Reproducción/fisiología , Medición de RiesgoRESUMEN
Loss of Dkk1 results in ectopic WNT/beta-catenin signalling activity in the anterior germ layer tissues and impairs cell movement in the endoderm of the mouse gastrula. The juxtaposition of the expression domains of Dkk1 and Wnt3 is suggestive of an antagonist-agonist interaction. The downregulation of Dkk1 when Wnt3 activity is reduced reveals a feedback mechanism for regulating WNT signalling. Compound Dkk1;Wnt3 heterozygous mutant embryos display head truncation and trunk malformation, which are not found in either Dkk1(+/-) or Wnt3(+/-) embryos. Reducing the dose of Wnt3 gene in Dkk1(-/-) embryos partially rescues the truncated head phenotype. These findings highlight that head development is sensitive to the level of WNT3 signalling and that DKK1 is the key antagonist that modulates WNT3 activity during anterior morphogenesis.