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Drainage developers

Authors
Journal
The Journal of Cell Biology
0021-9525
Publisher
The Rockefeller University Press
Publication Date
Identifiers
DOI: 10.1083/jcb.1853if
Keywords
  • News
  • In Focus
Disciplines
  • Agricultural Science
  • Biology

Abstract

untitled 373 In FocusText by Ruth Williams [email protected] IN FOCUS • THE JOURNAL OF CELL BIOLOGY Drainage developers O ur bodies’ tissues need contin- uous irrigation and drainage. Blood vessels feeding the tis- sues bring in the fl uids, and drainage occurs via the lymphatic system. Where- as much is known about how blood ves- sels are built, the same was not true for lymph vessels. Now though, Norrmén et al. have identifi ed two of the lead engi- neers that direct drainage construc- tion—the transcription factors, Foxc2 and NFATc1 (1). Previous studies found that mice lacking Foxc2 have malformed lymph vessels (2). Also, people with mutated Foxc2 suffer from severe limb swelling (lymphedema-distichiasis) caused by poor lymph drainage (3). Norrmén and colleagues have now found that Foxc2 specifi cally regulates a late stage of lymph development when large, valve- containing vessels arise from more primitive capillaries. One characteristic of the mal- formed vessels in Foxc2-defi cient mice is a lack of valves. “At the moment nothing is known [about] how lymphat- ic valves develop,” explained Tatiana Petrova, who led the study. The team there- fore turned to proteins known to build heart valves to look for can- didates that might co- operate with Foxc2 in the lymphatic system. Only one of these candidates, NFATc1, showed expression in the developing lymph system of normal mice, and the factor was particularly abundant in lymph vessel valves. Mice lacking NFATc1 die at an embryonic stage be- fore lymph valve formation—presum- ably due to failure of their heart and blood vessels, which develop earlier than the lymphatic system. To investi- gate the effect of NFATc1 on lymphatic valve development, the authors waited for normal mouse embryos to develop their circulatory system and then treated them with an NFAT inhibitor. The effect was very similar to that of mice that lack Foxc2. Supporting evidence for NFATc1’s involvement i

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