sall4 acts downstream of tbx5 and is required for pectoral fin outgrowth

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The role of SalU in vertebrate limb development

Genes required for limb developm ent have, in several instances, first been identified by studies of human diseases in which the limbs are affected. In humans, m utations in the transcription factor SALL4 results in Okihiro syndrome (OS), which is characterised by forelimb defects and the eye disorder, Duane anom aly. OS patients forelim b defects range from subtle thumb abnormalities to trunca...

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Mechanism of pectoral fin outgrowth in zebrafish development.

Fins and limbs, which are considered to be homologous paired vertebrate appendages, have obvious morphological differences that arise during development. One major difference in their development is that the AER (apical ectodermal ridge), which organizes fin/limb development, transitions into a different, elongated organizing structure in the fin bud, the AF (apical fold). Although the role of ...

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Tbx5 is dispensable for forelimb outgrowth.

Tbx5 is essential for initiation of the forelimb, and its deletion in mice results in the failure of forelimb formation. Misexpression of dominant-negative forms of Tbx5 results in limb truncations, suggesting Tbx5 is also required for forelimb outgrowth. Here we show that Tbx5 is expressed throughout the limb mesenchyme in progenitors of cartilage, tendon and muscle. Using a tamoxifeninducible...

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Distinct tissue-specific requirements for the zebrafish tbx5 genes during heart, retina and pectoral fin development

The transcription factor Tbx5 is expressed in the developing heart, eyes and anterior appendages. Mutations in human TBX5 cause Holt-Oram syndrome, a condition characterized by heart and upper limb malformations. Tbx5-knockout mouse embryos have severely impaired forelimb and heart morphogenesis from the earliest stages of their development. However, zebrafish embryos with compromised tbx5 func...

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TBX5 is required for embryonic cardiac cell cycle progression.

Despite the critical importance of TBX5 in normal development and disease, relatively little is known about the mechanisms by which TBX5 functions in the embryonic heart. Our present studies demonstrate that TBX5 is necessary to control the length of the embryonic cardiac cell cycle, with depletion of TBX5 leading to cardiac cell cycle arrest in late G(1)- or early S-phase. Blocking cell cycle ...

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ژورنال

عنوان ژورنال: Development

سال: 2006

ISSN: 1477-9129,0950-1991

DOI: 10.1242/dev.02259