scholarly journals OsARID3, an AT-rich Interaction Domain-containing protein, is required for shoot meristem development in rice

2015 ◽  
Vol 83 (5) ◽  
pp. 806-817 ◽  
Author(s):  
Yan Xu ◽  
Wei Zong ◽  
Xin Hou ◽  
Jialing Yao ◽  
Hongbo Liu ◽  
...  
2020 ◽  
Author(s):  
Sharma Nidhi ◽  
Liu Tie

AbstractIn Arabidopsis, the genes SHOOT MERISTEMLESS (STM) and CLAVATA3 (CLV3) antagonistically regulate shoot meristem development. STM is essential for both development and maintenance of the meristem, as stm mutants fail to develop a shoot meristem during embryogenesis. CLV3, on the other hand, negatively regulates meristem proliferation, and clv3 mutants possess an enlarged shoot meristem. Genetic interaction studies revealed that stm and clv3 dominantly suppress each other’s phenotypes. STM works in conjunction with its closely related homologue KNOTTED1-LIKE HOMEOBOX GENE 6 (KNAT6) to promote meristem development and organ separation, as stm knat6 double mutants fail to form a meristem and produce a fused cotyledon. In this study, we show that clv3 fails to promote post-embryonic meristem formation in stm-1 background if we also remove KNAT6. stm-1 knat6 clv3 triple mutants result in early meristem termination and produce fused cotyledons similar to stm knat6 double mutant. Notably, the stm-1 knat6 and stm-1 knat6 clv3 alleles lack tissue in the presumed region of SAM. stm knat6 clv3 also showed reduced inflorescence size and shoot apex size as compared to clv3 single or stm clv3 double mutants. In contrast to previously published data, these data suggest that stm is epistatic to clv3 in postembryonic meristem development.HighlightSTM and KNAT6 genes determine post-embryonic meristem formation and activity in Arabidopsis. clv3 mutation is unable to rescue the stm knat6 meristemless phenotype.


The Prostate ◽  
2021 ◽  
Author(s):  
Wataru Ikeuchi ◽  
Yuriko Wakita ◽  
Guoxiang Zhang ◽  
Chun Li ◽  
Keiichi Itakura ◽  
...  

2018 ◽  
Vol 9 (22) ◽  
pp. 4187-4196 ◽  
Author(s):  
Yuan Wang ◽  
Weiping Chang ◽  
Wanli Chang ◽  
Xiaowei Chang ◽  
Song Zhai ◽  
...  

2004 ◽  
Vol 279 (16) ◽  
pp. 16670-16676 ◽  
Author(s):  
Suhkmann Kim ◽  
Ziming Zhang ◽  
Sean Upchurch ◽  
Nancy Isern ◽  
Yuan Chen

2019 ◽  
Vol 117 (3) ◽  
pp. 1799-1805 ◽  
Author(s):  
Qingyu Wu ◽  
Fang Xu ◽  
Lei Liu ◽  
Si Nian Char ◽  
Yezhang Ding ◽  
...  

Heterotrimeric G proteins are important transducers of receptor signaling, functioning in plants with CLAVATA receptors in controlling shoot meristem size and with pathogen-associated molecular pattern receptors in basal immunity. However, whether specific members of the heterotrimeric complex potentiate cross-talk between development and defense, and the extent to which these functions are conserved across species, have not yet been addressed. Here we used CRISPR/Cas9 to knock out the maize G protein β subunit gene (Gβ) and found that the mutants are lethal, differing from those in Arabidopsis, in which homologous mutants have normal growth and fertility. We show that lethality is caused not by a specific developmental arrest, but by autoimmunity. We used a genetic diversity screen to suppress the lethal Gβ phenotype and also identified a maize Gβ allele with weak autoimmune responses but strong development phenotypes. Using these tools, we show that Gβ controls meristem size in maize, acting epistatically with G protein α subunit gene (Gα), suggesting that Gβ and Gα function in a common signaling complex. Furthermore, we used an association study to show that natural variation in Gβ influences maize kernel row number, an important agronomic trait. Our results demonstrate the dual role of Gβ in immunity and development in a cereal crop and suggest that it functions in cross-talk between these competing signaling networks. Therefore, modification of Gβ has the potential to optimize the trade-off between growth and defense signaling to improve agronomic production.


FEBS Letters ◽  
2019 ◽  
Vol 593 (19) ◽  
pp. 2716-2729 ◽  
Author(s):  
Aditi Maulik ◽  
Malyasree Giri ◽  
Mahavir Singh

2015 ◽  
Vol 43 (3) ◽  
Author(s):  
K. Lakshmi Jayaraj ◽  
U. Bhavyashree ◽  
T.P. Fayas ◽  
K.K. Sajini ◽  
M.K. Rajesh ◽  
...  

<div><table cellspacing="0" cellpadding="0" align="center"><tbody><tr><td align="left" valign="top"><p>Since coconut is   one of the most recalcitrant species to generate <em>in vitro</em>, it is   necessary to study in detail about the cellular changes that occur during   somatic embryogenesis to enhance our knowledge about this phenomenon. In the   present study, coconut plumular tissues, the shoot meristem including leaf   primordia, were used as explants for <em>in vitro </em>regeneration studies.   Histological studies were carried out in different stages of plumule culture.   No noticeable growth was observed in 15 days old cultures. After 30 days,   meristematic cells could be identified. Abundance of meristematic cells,   foremost to the development of callus structures, was observed after 45 days.   After 75 days, globular friable calli were formed and histological studies   revealed the presence of meristematic centers which eventually formed somatic   embryos. The histological study of matured somatic embryos formed after 120   days of callus initiation showed a clear meristematic zone of parenchyma   cells, surrounded by vascular bundles. Histological studies, carried out for   certain abnormalities like compact calli, abnormal somatic embryoids with   rudimentary shoots and multiplied roots, revealed the presence of intact   cotyledonary leaves which seemed to inhibit the apical meristem development   of somatic embryoids. The presence of vascular bundles in the early stages of   callus formation might lead to the direct formation of meristemoids. These   results could aid future studies leading to enhanced control of the somatic   embryogenic process and greater efficiency of somatic embryo and plantlet   formation in coconut.</p></td></tr></tbody></table></div>


2005 ◽  
Vol 19 (10) ◽  
pp. 2491-2501 ◽  
Author(s):  
Serban P. Georgescu ◽  
Joyce H. Li ◽  
Qing Lu ◽  
Richard H. Karas ◽  
Myles Brown ◽  
...  

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