NCBI Logo
GEO Logo
   NCBI > GEO > Accession DisplayHelp Not logged in | LoginHelp
GEO help: Mouse over screen elements for information.
          Go
Series GSE6179 Query DataSets for GSE6179
Status Public on Jan 22, 2007
Title An investigation into transcriptional changes in developing Arabidopsis leaf caused by novel signalling protein, SPH1.
Organism Arabidopsis thaliana
Experiment type Expression profiling by array
Summary Arabidopsis genome sequencing has revealed the presence of at least three extensive gene families that may encode protein ligands. One of these, the SPH (S-protein homologue) family, was identified as a direct result of our studies on self-incompatibility in Papaver. The Arabidopsis SPH gene family consists of 81 members. We have initiated experimental work on a subset of these. RT-PCR studies indicate that many, if not all, SPH genes are expressed. Each SPH gene encodes an N-terminal signal peptide sequence and thus SPH proteins are likely to be secreted. Until recently none of the genes in this family had known function. However we have evidence that one member of the family, SPH1 is involved in leaf vascular development. In order to determine the function of SPH1, Arabidopsis plants were transformed with an SPH1 antisense construct. Analysis of the mutant phenotype shows that whilst plants appear as wt until principal growth stage 1.04, they subsequently show severe morphological defects. Plants are severely dwarfed with twisted rosette leaves at ~ 30% wt length and width as well as shortened inflorescence stem. Closer examination revealed aberrant leaf vasculature and severe reduction in expansion of parenchyma cells surrounding the primary leaf vein. We have conducted preliminary immunolocalisation studies with antibody raised to SPH1. These suggest that SPH1 protein is secreted by cells within the developing vasculature of the immature leaf (leaves<6mm in length). The data that we have so far obtained leads us to believe that SPH1 protein acts as a signalling molecule during early leaf development. As SPH1 is likely to be a signalling protein it is assumed that its interaction with a cognate receptor results in initiation of developmental processes within leaf tissue. The purpose of the experiment is to determine the network of genes within the normally developing rosette leaf whose expression is altered by SPH1. This will be accomplished by comparing transcriptional levels in rosette leaves of antisense-SPH1 plants with wt plants. We propose to make target RNA from rosette leaves taken from plants at principal stage 1.05 (immediately after initial appearance of developmental abnormality) and from plants at principal stage 1.14 (where gross changes are apparent). We propose to use replicate slides for each hybridisation, i.e. 2 hybridised to RNA from wt leaves at 1.05, 2 antisense at 1.05, 2 wt at 1.14 and 2 antisense at 1.14.
Keywords: genetic_modification_design
 
Overall design Number of plants pooled:40
 
Contributor(s) Wheeler M
Citation missing Has this study been published? Please login to update or notify GEO.
Submission date Oct 27, 2006
Last update date Aug 28, 2018
Contact name Nottingham Arabidopsis Stock Centre (NASC)
E-mail(s) [email protected]
Phone +44 (0)115 951 3237
Fax +44 (0)115 951 3297
URL http://arabidopsis.info/
Organization name Nottingham Arabidopsis Stock Centre (NASC)
Department School of Biosciences, University of Nottingham
Street address Sutton Bonington Campus
City Loughborough
ZIP/Postal code LE12 5RD
Country United Kingdom
 
Platforms (1)
GPL198 [ATH1-121501] Affymetrix Arabidopsis ATH1 Genome Array
Samples (12)
GSM142886 MW001_ATH1_A1-Wheel-a05
GSM142887 MW001_ATH1_A1-Wheel-a14
GSM142888 MW001_ATH1_A1-Wheel-w05
Relations
Affiliated with GSE69995
BioProject PRJNA100647

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE6179_RAW.tar 28.0 Mb (http)(custom) TAR (of CEL)

| NLM | NIH | GEO Help | Disclaimer | Accessibility |
NCBI Home NCBI Search NCBI SiteMap