scholarly journals ALTERED MERISTEM PROGRAM1 regulates leaf identity independent of miR156-mediated translational repression

2019 ◽  
Author(s):  
Jim P. Fouracre ◽  
Victoria J. Chen ◽  
R. Scott Poethig

AbstractIn Arabidopsis, loss of the carboxypeptidase, ALTERED MERISTEM PROGRAM1 (AMP1), produces an increase in the rate of leaf initiation, an enlarged shoot apical meristem and an increase in the number of juvenile leaves. This phenotype is also observed in plants with reduced levels of miR156-targeted SQUAMOSA PROMOTER BINDING PROTEIN-LIKE (SPL) transcription factors, suggesting that AMP1 may promote SPL activity. However, we found that the amp1 phenotype is only partially corrected by elevated SPL gene expression, and that amp1 has no significant effect on SPL transcript levels, or on the level or the activity of miR156. Although evidence from a previous study suggests that AMP1 promotes miRNA-mediated translational repression, amp1 did not prevent the translational repression of the miR156 target, SPL9, or the miR159 target, MYB33. These results suggest that AMP1 regulates vegetative phase change downstream of, or in parallel to, the miR156/SPL pathway and that it is not universally required for miRNA-mediated translational repression.Summary statementWe show that loss of the carboxypeptidase, AMP1, does not interfere with the function of miR156 or miR159, suggesting that AMP1 is not universally required for miRNA-mediated translational repression in Arabidopsis.

2019 ◽  
Vol 116 (20) ◽  
pp. 10168-10177 ◽  
Author(s):  
Jim P. Fouracre ◽  
R. Scott Poethig

The extent to which the shoot apical meristem (SAM) controls developmental decisions, rather than interpreting them, is a longstanding issue in plant development. Previous work suggests that vegetative phase change is regulated by signals intrinsic and extrinsic to the SAM, but the relative importance of these signals for this process is unknown. We investigated this question by examining the effect of meristem-deficient mutations on vegetative phase change and on the expression of key regulators of this process, miR156 and its targets, SPL transcription factors. We found that the precocious phenotypes of meristem-deficient mutants are a consequence of reduced miR156 accumulation. Tissue-specific manipulation of miR156 levels revealed that the SAM functions as an essential pool of miR156 early in shoot development, but that its effect on leaf identity declines with age. We also found that SPL genes control meristem size by repressing WUSCHEL expression via a novel genetic pathway.


PLoS Genetics ◽  
2007 ◽  
Vol 3 (6) ◽  
pp. e101 ◽  
Author(s):  
Xiaolan Zhang ◽  
Shahinez Madi ◽  
Lisa Borsuk ◽  
Dan Nettleton ◽  
Robert J Elshire ◽  
...  

2015 ◽  
Vol 62 (5) ◽  
pp. 684-694 ◽  
Author(s):  
M. Wu ◽  
J. Li ◽  
S. L. Fan ◽  
M. Z. Song ◽  
C. Y. Pang ◽  
...  

1993 ◽  
Vol 5 (3) ◽  
pp. 297-309 ◽  
Author(s):  
A J Fleming ◽  
T Mandel ◽  
I Roth ◽  
C Kuhlemeier

2021 ◽  
Author(s):  
Jim P. Fouracre ◽  
Jia He ◽  
Victoria J. Chen ◽  
Simone Sidoli ◽  
R. Scott Poethig

SummaryHow organisms control when to transition between different stages of development is a key question in biology. In plants, epigenetic silencing by Polycomb repressive complex 1 (PRC1) and PRC2 plays a crucial role in promoting developmental transitions, including from juvenile-to-adult phases of vegetative growth. It is well established that PRC1/2 repress the master regulator of vegetative phase change, miR156, leading to the transition to adult growth, but how this process in temporally regulated is unknown. Here we investigate whether transcription factors in the VIVIPAROUS/ABI3-LIKE (VAL) gene family provide the temporal signal for the epigenetic repression of miR156. Exploiting a novel val1 allele, we found that VAL1 and VAL2 redundantly regulate vegetative phase change by controlling the overall level, rather than temporal dynamics, of miR156 expression. Furthermore, we discovered that VAL1 and VAL2 also act independently of miR156 to control this important developmental transition.


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