Cx43 suppresses evx1 expression to regulate joint initiation in the regenerating fin.
Cx43 suppresses evx1 expression to regulate joint initiation in the regenerating fin.
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DOI:
10.1002/dvdy.24531
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发表时间:
2017-09
期刊:
影响因子:
--
通讯作者:
Iovine MK
中科院分区:
文献类型:
--
作者:
Dardis G;Tryon R;Ton Q;Johnson SL;Iovine MK
How joints are correctly positioned in the vertebrate skeleton remains poorly understood. From our studies on the regenerating fin, we have evidence that the gap junction protein Cx43 suppresses joint formation by suppressing the expression of the evx1 transcription factor. Joint morphogenesis proceeds through at least two discrete stages. First, cells that will produce the joint condense in a single row on the bone matrix (“initiation”). Second, these cells separate coincident with articulation of the bone matrix. We propose that Cx43 activity is transiently reduced prior to joint initiation. We first define the timing of joint initiation with respect to regeneration. We next correlate reduced cx43 expression and increased evx1 expression with initiation. Through manipulation of cx43 expression we demonstrate that Cx43 negatively influences evx1 expression and joint formation. We further demonstrate that Cx43 activity in the dermal fibroblasts is required to rescue joint formation in the cx43 mutant, short fin b123. We conclude that Cx43 activity in the dermal fibroblasts influences the expression of evx1, and therefore the differentiation of the precursor cells that give rise to the joint-forming osteoblasts.
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影响因子:
11.8
作者:
Knopf, Franziska;Hammond, Christina;Weidinger, Gilbert
通讯作者:
Weidinger, Gilbert
影响因子:
2.7
作者:
Sims, Kenneth, Jr.;Eble, Diane M.;Iovine, M. Kathryn
通讯作者:
Iovine, M. Kathryn
影响因子:
2.7
作者:
Hoptak-Solga, Angela D.;Nielsen, Sarah;Iovine, M. Kathryn
通讯作者:
Iovine, M. Kathryn
DOI:
10.1196/annals.1346.010
发表时间:
2006-01-01
期刊:
SKELETAL DEVELOPMENT AND REMODELING IN HEALTH, DISEASE, AND AGING
影响因子:
--
作者:
Pacifici, Maurizio;Koyama, Eiki;Iwamoto, Masahiro
通讯作者:
Iwamoto, Masahiro
影响因子:
2.7
作者:
Ton QV;Kathryn Iovine M
通讯作者:
Kathryn Iovine M