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ARS Home » Pacific West Area » Albany, California » Plant Gene Expression Center » Research » Publications at this Location » Publication #135554
Title: DEPENDENCE OF STEM CELL FATE IN ARABIDOPSIS ON A FEEDBACK LOOP REGULATED BY CLV3 ACTIVITY

Author
item BRAND, ULRIKE - UNIV OF COLOGNE, GERMANY
item Fletcher, Jennifer
item HOBE, MARTIN - UNIV OF COLOGNE, GERMANY
item MEYEROWITZ, ELLIOTT - CALIF INSTIT OF TECHNOLOG
item SIMON, RUDIGER - UNIV OF COLOGNE, GERMANY

Submitted to: Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/25/2000
Publication Date: 7/28/2000
Citation: N/A

Interpretive Summary: This article reports results important new data on how a gene called CLAVATA3 (CLV3) functions in Arabidopsis development. CLV3 encodes a signaling molecular that prevents the stem cells at the growing tip of the Arabidopsis plant from becoming larger than normal and producing extra stem and flower tissue. We generated and analyzed transgenic plants that express CLV3 at artificially high levels, finding that the amount of CLV3 made in the plant directly affects the number of stem cells that are formed. We also demonstrated that CLV3 signaling is one element of a feedback loop that acts to prevent the growing tip from generating too many or too few cells. The discovery of this type of feedback loop in plants allows us for the first time to model how plants are able to produce organs throughout their lives by maintaining pools of stem cells at their growing tips.

Technical Abstract: The fate of stem cells in plant meristems is governed by directional signalling systems that are regulated by negative feedback. In Arabidopsis, the CLAVATA (CLV) genes encode the essential components of a negative, stem cell restricting pathway. We have used transgenic plants over-expressing CLV3 to show that meristem cell accumulation and fate depends directly on the level of CLV3 activity, and that CLV3 signalling occurs exclusively through a CLV1/CLV2 receptor kinase complex. We also demonstrate that the CLV pathway acts by repressing the activity of the transcription factor WUSCHEL, an element of the positive, stem cell promoting pathway.