tailieunhanh - báo cáo khoa học: " pax1-1 partially suppresses gain-of-function mutations in Arabidopsis AXR3/IAA17"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: pax1-1 partially suppresses gain-of-function mutations in Arabidopsis AXR3/IAA17 | BMC Plant Biology BioMed Central Research article paxl-l partially suppresses gain-of-function mutations in Arabidopsis AXR3 IAAI7 Mimi Tanimoto1 2 Jemma Jowett1 3 Petra Stirnberg1 Dean Rouse1 4 and Ottoline Leyser 1 Open Access Address Department of Biology University of York Heslington York YO10 5YW UK 2Department of Molecular and Cellular Biology Axelrod Building University of Guelph Guelph Ontario N1G 2W1 Canada 3Section of Molecular and Cellular Biology University of California Davis One Shields Avenue Davis CA 95616 USA and 4Research School of Biological Science GPO Box 475 Canberra ACT 2601 Australia Email Mimi Tanimoto - htanimot@ Jemma Jowett - jjowett@ Petra Stirnberg - ps25@ Dean Rouse - rouse@ Ottoline Leyser - hmol1@ Corresponding author Published 12 April 2007 Received 6 November 2006 BMC Plant Biology 2007 7 20 doi 1471-2229-7-20 Accepted 12 April 2007 This article is available from http 1471-2229 7 20 2007 Tanimoto et al licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License http licenses by which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract_ Background The plant hormone auxin exerts many of its effects on growth and development by controlling transcription of downstream genes. The Arabidopsis gene AXR3 IAA17 encodes a member of the Aux IAA family of auxin responsive transcriptional repressors. Semi-dominant mutations in AXR3 result in an increased amplitude of auxin responses due to hyperstabilisation of the encoded protein. The aim of this study was to identify novel genes involved in auxin signal transduction by screening for second site mutations that modify the axr3-1 gain-of-function phenotype. .

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