Project description:pin1 mutnat doesn't produce any floral organs, which can be rescued by exogenous application of IAA paste. Here we applied exogenous IAA paste and collected meristem tissue after different time points (30 min, 4hr, 12hr, 16hr). As a control we applied mock paste. Around 10 meristems were dissected under dissecting scope for each biological replicate. Some known IAA inducible genes were checked for their upregulation in extracted RNA, and there after the RNA was sequenced.
Project description:Arabidopsis thaliana mutant sr45-1 has an altered flower shape. sr45 is a splicing regulator. In this study, we examined the proteins from inflorescence of sr45-1 mutant plants and wild-type. Wild type TMT labels: 126, 128, 130. sr45-1 TMT labels: 127, 129, 131.
Project description:We report the application of laser capture microdissection (LCM) for high resolution transcriptome profiling of the second internode of the Arabidopsis thaliana inflorescence stem. In this series, we used LCM to determine and compare the transcriptome profiles of the phloem cap, the pith, and the remaining vascular bundle area.
Project description:Null mutations of tomato FRUITFULL-like genes FUL1, FUL2, MBP10, MBP20 caused delayed flowering and branched inflorescence, so we sequenced mRNA from vegetative meristems (VM), transition meristems (TM), floral meristems (FM), and FM of the first sympodial shoot of tomato mutant ful1/ful2/mbp10/mbp20 (slful) as well as the wild type Moneyberg (WT) to see genome-wide expression changes affected by the mutations.
Project description:Transcriptional profiling of cotyledon transcriptomics at the seedling stage (6 d) by comparison of wild-type vs. cotyledon-less laterne (= pid enp) homozygous mutant. The goal was to determine the transcriptomic profile of a cotyledon. The experiment took advantage of the endogenously caused lack of cotyledons instead of dissecting these organs, which would cause wound-induced expression.This was achieved by comparing seedlings of the Arabidopsis thaliana pid enp double mutant, which is incapable to generate cotyledons. This is caused by the loss of apical cell polarisation of the auxin efflux carrier PIN1 in epidermal cells during embryogenesis.
