Summary of Study ST002571
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001658. The data can be accessed directly via it's Project DOI: 10.21228/M8CX2C This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
| Study ID | ST002571 |
| Study Title | Quantification of cytokinins in ap1 cal AP1-GR and drmy1 ap1 cal AP1-GR inflorescences using LC-MS |
| Study Type | Quantification using mass spectrometry |
| Study Summary | Robustness is the invariant development of phenotype despite environmental changes and genetic perturbations. In the Arabidopsis flower bud, four sepals initiate at robust positions and times and grow to equal size to enclose and protect the inner floral organs. We previously characterized the mutant development related myb-like1 (drmy1), where 3-5 sepals initiate at irregular positions and variable times and grow to different sizes, compromising their protective function. This loss of robustness was caused by a uniform increase in cytokinin signaling, as revealed by the TCS::GFP reporter, in the floral meristem before sepal initiation. We hypothesized that the increase in cytokinin signaling in drmy1 was due to an increase in the level of cytokinins. To test this idea, we extracted cytokinins from induced inflorescences of wild-type (5 bio-reps) and drmy1 (6 bio-reps) in ap1 cal AP1-GR background. We measured the level of three cytokinin bases, trans-Zeatin (tZ), cis-Zeatin (cZ), and isopentenyladenine (iP), and their corresponding nucleosides (tZR, cZR, and iPR), using liquid chromatography-mass spectrometry. We found that there was no statistically significant differences in cytokinin levels between these genotypes, indicating that the increase in cytokinin signaling in the drmy1 floral meristem is not due to increased cytokinin levels. |
| Institute | Cornell University |
| Department | Plant Biology Section |
| Laboratory | Roeder Lab |
| Last Name | Kong |
| First Name | Shuyao |
| Address | 239 Weill Hall, 526 Campus Road, Ithaca, NY 14853 |
| sk3245@cornell.edu | |
| Phone | 6072629684 |
| Submit Date | 2023-04-20 |
| Num Groups | 2 |
| Total Subjects | 11 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | raw(Thermo) |
| Analysis Type Detail | LC-MS |
| Release Date | 2023-05-11 |
| Release Version | 1 |
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Project:
| Project ID: | PR001658 |
| Project DOI: | doi: 10.21228/M8CX2C |
| Project Title: | DRMY1 promotes robust morphogenesis by sustaining translation of a hormone signaling protein |
| Project Type: | MS quantitative analysis |
| Project Summary: | Robustness is the invariant development of phenotype despite environmental changes and genetic perturbations. In the Arabidopsis flower bud, four sepals initiate at robust positions and times and grow to equal size to enclose and protect the inner floral organs. We previously characterized the mutant development related myb-like1 (drmy1), where 3-5 sepals initiate at irregular positions and variable times and grow to different sizes, compromising their protective function. The molecular mechanism underlying this loss of robustness was unclear. Here, we show that drmy1 has reduced TARGET OF RAPAMYCIN (TOR) activity, ribosomal content, and translation. Translation reduction decreases the protein level of ARABIDOPSIS RESPONSE REGULATOR7 (ARR7), a rapidly synthesized and degraded cytokinin signaling inhibitor. The resultant upregulation of cytokinin signaling disrupts the robust positioning of auxin signaling, causing variable sepal initiation. Our work shows that the homeostasis of translation, a ubiquitous cellular process, is crucial for the robust spatiotemporal patterning of organogenesis. |
| Institute: | Cornell University |
| Department: | Plant Biology Section |
| Laboratory: | Roeder Lab |
| Last Name: | Kong |
| First Name: | Shuyao |
| Address: | 239 Weill Hall, 526 Campus Road, Ithaca, NY, 14850, USA |
| Email: | sk3245@cornell.edu |
| Phone: | 6072629684 |
| Funding Source: | Research reported in this publication was supported by the National Institute of General Medical Sciences of the National Institutes of Health (NIH) under award numbers R01GM134037 (A.H.K.R.), DP5OD023072 (J.O.B.), and R01GM145814 (J.O.B.); Cornell Graduate School new student fellowship (S.K.); and in part by a Schmittau-Novak Grant from the School of Integrative Plant Science, Cornell University (M.Z.). H.G.G. was supported by NIH Director’s New Innovator Award (DP2 OD024541-01) and NSF CAREER Award (1652236), NIH R01 Award (R01GM139913), and the Koret-UC Berkeley-Tel Aviv University Initiative in Computational Biology and Bioinformatics. H.G.G. is also a Chan Zuckerberg Biohub Investigator. |
| Contributors: | Shuyao Kong, Mingyuan Zhu, M. Regina Scarpin, David Pan, Longfei Jia, Ryan E. Martinez, Simon Alamos, Batthula Vijaya Lakshmi Vadde, Hernan G. Garcia, Shu-Bing Qian, Jacob O. Brunkard, Adrienne H. K. Roeder |
