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c-jun Is dispensable for developmental cell death and axogenesis in the retina
K H Herzog1, S C Chen, J I Morgan
1Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105, USA.
Abstract:
Although a number of studies have implicated c-Jun in neuronal death and axonal regeneration, it is unknown whether Jun function is essential for either response. One approach to resolve this issue is to analyze knock-out mice. However, c-jun-null mice die at midgestation, precluding critical investigation. Therefore, a xenograft paradigm was used in which retinas from embryonic day 12.5 (E12.5) c-jun nullizygous or wild-type mice were transplanted onto the superior colliculus of newborn rats. The rats were allowed to develop, and the grafts were assayed at various times for cell death and axon growth. Histologically, grafts of both genotypes developed in identical manners and had morphological characteristics of retinas. A functional c-jun allele was not essential for axogenesis, because ganglion cells in retinal grafts from c-jun nullizygous mice developed axons that projected into the colliculus. Programmed cell death (PCD) was also evident in the age-appropriate regions of the retina in both wild-type and c-jun-null grafts. Furthermore, there were no discernible differences in the number or location of dying cells in the two genotypes. That c-jun was not essential for PCD was supported by two additional findings. First, a c-jun-lacZ reporter gene was expressed in many cells in developing and grafted retinas, although only a few of these cells were destined to die. Second, in E12.5 c-jun-null embryos there were normal levels of PCD in the trigeminal ganglion. Together, these data indicate that c-Jun is not essential for axon growth in the retina or for PCD in the retina and trigeminal ganglion.
Insights
This study found that c-Jun is not essential for retinal axon growth or programmed cell death (PCD). Researchers used a xenograft model to investigate c-Jun
Area of Science:
- Neuroscience
- Developmental Biology
- Molecular Biology
Background:
- c-Jun is implicated in neuronal death and axonal regeneration.
- The essentiality of c-Jun function for these neuronal responses remains unclear.
- c-jun-null mice exhibit midgestation lethality, hindering direct investigation.
Purpose of the Study:
- To determine if c-Jun function is essential for retinal axon growth and programmed cell death (PCD).
- To investigate the role of c-Jun in neuronal development using a xenograft model.
Main Methods:
- A xenograft paradigm was employed, transplanting embryonic day 12.5 (E12.5) retinas from c-jun nullizygous or wild-type mice onto the superior colliculus of newborn rats.
- Grafts were analyzed for cell death and axon growth at various time points post-transplantation.
- Expression of a c-jun-lacZ reporter gene and PCD levels in the trigeminal ganglion were also assessed.
Main Results:
- Retinal grafts from both c-jun nullizygous and wild-type mice developed similarly, exhibiting characteristic retinal morphology.
- Ganglion cells in c-jun nullizygous retinal grafts successfully developed axons that projected into the rat superior colliculus, indicating axogenesis is not dependent on c-Jun.
- Programmed cell death (PCD) occurred in both genotypes without discernible differences in cell number or location; c-Jun expression was observed in many cells, but not exclusively in dying cells.
Conclusions:
- c-Jun is not essential for axogenesis in the developing retina.
- c-Jun is not essential for programmed cell death (PCD) in the retina or trigeminal ganglion.
- These findings clarify the non-essential role of c-Jun in specific neuronal developmental processes.