INVESTIGADORES
AYBAR Manuel Javier
congresos y reuniones científicas
Título:
Implications of mef2c in the early development of Xenopus laevis
Autor/es:
MARIA EUGENIA PEREZ COLLADO; MARCELA BONANO; GABRIELA MARRANZINO; MANUEL J. AYBAR
Lugar:
Santiago
Reunión:
Simposio; International Symposium Visualisation and manipulation of signals and forces in developing tissues; 2014
Institución organizadora:
Biomedical Neuroscience Institute, ICM, Chile
Resumen:
The neural crest is
unique for the Vertebrate organisms, consists of a cell population that is
highly migratory and gives rise to a wide variety of derived tissues. Neural
crest development is regulated by the interaction of several genes that form a
genetic network. The hierarchical relationships between some components of this
complex network as well as the gene functions have already been established but
there is much information that has to be enlightened. In a previous work, we
demonstrated that the cell signaling pathway mediated by the Endothelin
Receptor A (Ednra) is required for the neural crest development in the
amphibian Xenopus laevis,
from its induction to the proper formation of some derivatives, just like the
melanocytes and the cranial cartilages. Nevertheless, to date there is
fragmented information about the genes that activate when the ligand Endothelin
1 (Edn1) binds to its specific membrane receptor Ednra. In the present study,
we identify the gene mef2c (myocyte enhancer factor 2 c) as a plausible
candidate of target genes that are activated through the Edn1/Ednra cell
signaling pathway in X. laevis.
The expression of mef2c was characterized in a previous work.
However, we found some differences. The beginning of its expression is first
detected by whole mount in situ hybridization at mid neurula stages (St. 15-16)
in axial and paraxial mesoderm as well as in neural folds. As embryonic
development progresses, mef2c expresses in the cranial migratory
streams of the neural crest and further, in the branchial arches, muscle mass
of the head, in the heart and in the somites. The loss-of-function approaches
suggest that mef2c is downstream of ednra in the genetic cascade that guides the
neural crest development. When the function of ednra is suppressed through the
microinjection of a specific morpholino oligonucleotide (MO-ednra), the
expression of mef2c appears irregular, evidencing a
disorder in the cranial streams of the migratory neural crest. Similar results
are observed with the pharmacological blockade using BQ123, a specific
inhibitor of Ednra. This disorganization is absent when mef2c mRNA is coinjected with MO-ednra proving that mef2c is able to rescue the normal phenotype
of the cranial streams. Moreover, the
bioinformatics studies demonstrate that the aminoacidic sequence of Mef2c
proteins is conserved between the vertebrates. This fact, in addition to the
evidences that mef2c is regulated by the Edn1/Ednra pathway
in the development of the jaw in Danio
rerio, suggests that in the vertebrates embryos mef2c could be implied in processes of
neural crest formation and that its expression is controlled by the signaling
mediated by Edn1/Ednra.