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1 apical nodes of the stalk because of loss of apical dominance.
2 ion, abnormal vein patterning, and decreased apical dominance.
3 owth of axillary buds, a phenomenon known as apical dominance.
4 ient for suppressed buds to be released from apical dominance.
5 d morphology, including dwarfism and reduced apical dominance.
6 ot apex-produced auxin, a mechanism known as apical dominance.
7 increases in petiole length, leaf angle and apical dominance.
8 s are late to nonflowering, and show reduced apical dominance.
9 calized production of ROS and enforcement of apical dominance.
10 ing hypocotyl elongation, leaf expansion and apical dominance.
11 rved in axillary buds following release from apical dominance.
12 ncluding increased plant height and enhanced apical dominance.
13 lude stunting, leaf curling, and the loss of apical dominance.
14 ypocotyl elongation at high temperature, and apical dominance.
15 aves, short inflorescence stems, and reduced apical dominance.
16 levels of NtPSA1 mRNA and exhibited reduced apical dominance.
17 radius, flowering time, stem elongation, and apical dominance.
18 ial trichome initiation, flowering time, and apical dominance.
19 g time, abaxial leaf trichome initiation and apical dominance.
20 ng a possible link with the observed loss of apical dominance.
21 lateral organs, which led to the concept of apical dominance.
22 the axillary buds below it, contributing to apical dominance.
24 er in the search for key factors controlling apical dominance,(2)(,)(3) identifying critical roles fo
25 ced levels of POTM1 mRNA exhibited decreased apical dominance accompanied by a compact growth habit a
27 effects including enhanced shooting, reduced apical dominance and delayed senescence and flowering.
29 enesis of lateral organs in the shoot, shoot apical dominance and growth, phyllotaxis, and lateral or
30 and elevated CO(2) level resulted in loss of apical dominance and rapid necrosis in glyphosate-treate
32 severe dwarfism, dark green leaves, reduced apical dominance, and altered photomorphogenesis, resemb
33 an defects, low fertility, dwarfism, loss of apical dominance, and altered responses to multiple plan
35 nt hormone that regulates plant development, apical dominance, and growth-related tropisms, such as p
37 h, reduced elongation of internodes, reduced apical dominance, and reduced leaf size and complexity.
38 developmental responses, including tropisms, apical dominance, and rhizoid initiation, which are subj
39 , thickened leaves; males sterility; reduced apical dominance; and de-etiolation of dark-grown seedli
40 addition, tir3 plants display a reduction in apical dominance as well as decreased elongation of sili
41 is indicates a role of SAD1 in regulation of apical dominance by modulation of branching through incr
43 mays), which exhibits a profound increase in apical dominance compared with its probable wild ancesto
44 ted crop plants have been bred for increased apical dominance, displaying greatly reduced axillary br
45 ow pleiotropic phenotypes, including reduced apical dominance, elongated life span and flowering dura
46 pmental defects, including dwarfism, reduced apical dominance, extreme longevity, dark-green leaves,
47 th habit, including reduced stature, loss of apical dominance, highly branched inflorescences and fru
48 expression of silenced genes, suppression of apical dominance, homeotic changes, heterochronic shift
49 ression and partially explains the increased apical dominance in maize compared to its progenitor, te
50 he tb1 gene largely controls the increase in apical dominance in maize relative to teosinte, and a re
51 biosynthesis acts as a pivotal regulator of apical dominance in moss and constitutes a shared mechan
52 esis that shoot inversion-induced release of apical dominance in Pharbitis nil is due to gravity stre
57 While the impact of hormonal regulation on apical dominance is well characterized, the prime import
59 s in several classic auxin responses such as apical dominance, lateral root initiation, sensitivity t
60 entiation of pin-like inflorescence, loss of apical dominance, leaf fusion, and reduced root growth.
61 hology, including shorter stature, increased apical dominance, leaf hyponasty, and inhibition of leaf
62 Here, we report an AtMYB2-regulated post apical dominance mechanism by which Arabidopsis (Arabido
63 stems are an option to handle the pronounced apical dominance of grapevines and to influence diverse
64 and ron3-2 mutant phenotypes [i.e., reduced apical dominance, primary root length, lateral root emer
67 ore generally, the extent of conservation in apical dominance regulation within the land plants remai
68 leading to the hypothesis that release from apical dominance relies on an increased supply of CK to
70 yed senescence, suppression of auxin-induced apical dominance, signaling of nitrogen availability, di
71 es, including defective root growth, loss of apical dominance, sterility, and homeotic floral transfo
72 enotypes, dwarfism, delayed flowering and no apical dominance, suggesting a global role for CHB2 in t
73 rop plants has often involved an increase in apical dominance (the concentration of resources in the
75 that leafy shoot apex decapitation releases apical dominance through massive and rapid transcription
76 or root and shoot growth, stomata formation, apical dominance, transition to flowering, and male game
78 ated bud inhibition, allowing buds to escape apical dominance under favourable conditions, such as hi
81 ormone auxin has been central to theories on apical dominance, whereby the growing shoot tip suppress
82 responsible for S. reilianum-induced loss of apical dominance, which we named SUPPRESSOR OF APICAL DO
83 ne resulted in reduced vegetative growth and apical dominance with abnormal development of flowers.