scholarly journals Repression of lateral organ boundary genes by PENNYWISE and POUND-FOOLISH is essential for meristem maintenance and flowering in Arabidopsis thaliana1

2015 ◽  
pp. pp.00915.2015 ◽  
Author(s):  
Madiha Khan ◽  
Laura Ragni ◽  
Paul Tabb ◽  
Brenda C Salasini ◽  
Steven Chatfield ◽  
...  
2006 ◽  
Vol 18 (3) ◽  
pp. 574-585 ◽  
Author(s):  
Esteban Bortiri ◽  
George Chuck ◽  
Erik Vollbrecht ◽  
Torbert Rocheford ◽  
Rob Martienssen ◽  
...  

2011 ◽  
Vol 23 (10) ◽  
pp. 3671-3683 ◽  
Author(s):  
Barbara Berckmans ◽  
Valya Vassileva ◽  
Stephan P.C. Schmid ◽  
Sara Maes ◽  
Boris Parizot ◽  
...  

Development ◽  
1997 ◽  
Vol 124 (16) ◽  
pp. 3045-3054 ◽  
Author(s):  
R.A. Kerstetter ◽  
D. Laudencia-Chingcuanco ◽  
L.G. Smith ◽  
S. Hake

The product of the maize homeobox gene, knotted1 (kn1), localizes to the nuclei of cells in shoot meristems, but is absent from portions of the meristem where leaf primordia or floral organs initiate. Recessive mutant alleles of kn1 were obtained by screening for loss of the dominant leaf phenotype in maize. Mutant kn1 alleles carrying nonsense, splicing and frame shift mutations cause severe inflorescence and floral defects. Mutant tassels produce fewer branches and spikelets. Ears are often absent, and when present, are small with few spikelets. In addition, extra carpels form in female florets and ovule tissue proliferates abnormally. Less frequently, extra leaves form in the axils of vegetative leaves. These mutations reveal a role for kn1 in meristem maintenance, particularly as it affects branching and lateral organ formation.


2019 ◽  
Author(s):  
Satoshi Naramoto ◽  
Victor Arnold Shivas Jones ◽  
Nicola Trozzi ◽  
Mayuko Sato ◽  
Kiminori Toyooka ◽  
...  

AbstractLand plant shoot structures evolved a diversity of lateral organs as morphological adaptations to the terrestrial environment, in which lateral organs independently evolved in each lineage in the sporophyte or gametophyte generation. The gametophyte meristem of the basally-diverging plant Marchantia polymorpha produces axes with non-photosynthetic scale-like lateral organs instead of leaves. Here we report that an ALOG (Arabidopsis LSH1 and Oryza G1) family protein in Marchantia, MpTAWAWA1 (MpTAW1), regulates meristem maintenance and lateral organ development. A mutation in MpTAW1, preferentially expressed in lateral organs, induces lateral organs with mis-specified identity and increased cell number, and furthermore, causes defects in apical meristem maintenance. Remarkably, MpTAW1 expression rescued the elongated-spikelet phenotype of a rice mutant of MpTAW1 homologue. This suggests that ALOG genes are co-opted to specify lateral organ identities in both gametophyte and sporophyte shoots by repressing lateral organ growth. We propose that the recruitment of ALOG-mediated lateral organ modification was in part responsible for the convergent evolution of independently-evolved lateral organs among highly divergent plant lineages and contributed to the morphological diversification of land plants.


Development ◽  
2002 ◽  
Vol 129 (8) ◽  
pp. 1957-1965 ◽  
Author(s):  
Mary E. Byrne ◽  
Joseph Simorowski ◽  
Robert A. Martienssen

The shoot apical meristem comprises undifferentiated stem cells and their derivatives, which include founder cells for lateral organs such as leaves. Meristem maintenance and lateral organ specification are regulated in part by negative interactions between the myb domain transcription factor ASYMMETRIC LEAVES1, which is expressed in lateral organ primordia, and homeobox transcription factors which are expressed in the shoot apical meristem (knox genes). The knox gene SHOOT MERISTEMLESS (STM) negatively regulates ASYMMETRIC LEAVES1 (AS1) which, in turn, negatively regulates other knox genes including KNAT1 and KNAT2, and positively regulates the novel gene LATERAL ORGAN BOUNDARIES (LOB). Genetic interactions with a second gene, ASYMMETRIC LEAVES2 (AS2), indicate it acts at the same position in this hierarchy as AS1. We have used a second-site suppressor screen to isolate mutations in KNAT1 and we show that KNAT1 is partially redundant with STM in regulating stem cell function. Mutations in KNAT2 show no such interaction. We discuss the regulation and evolution of redundancy among knox genes.


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