Seed dormancy breaking mechanisms.ppt/slideshare/Dr. K. Vanangamudi
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SEED DORMANCY
BREAKING
MECHANISMS
K.VANANGAMUDI
Formerly Dean (Agriculture), AC & RI, Coimbatore
Dean, Adhiparasakthi Agricultural College, Kalavai
Professor & Head, Seed Science & Technology
Tamil Nadu Agricultural University,
Coimbatore 641 003
Tamil Nadu
CELL WALL
H+ H+
H+
H+
H+
H+
H+
H+
H+
ATP PLASMA MEMBRANE
Plasma
membrane
Cell
wall
Nucleus
Vacuole
Cytoplasm
H2O
CYTOPLASM
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A plant hormone is any chemical that is produced
in one part of the plant that has a targeted function
elsewhere.
•“Classic” plant hormone
Auxin, CKs, GAs, Ethylene, and ABA
•“New" plant hormones
Brassinosteroids and Salicylic Acids
•Certain hormones induce dormancy, while others
break dormancy and initiate germination
•ABA plays a direct role.
•Ethylene and gibberellins are indirectly involved.
HORMONAL REGULATION OF DORMANCY
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Role of hormones in dormancy
and germination control
Relationship GA CK ABA Response
1 + + ‐ Germination
2 + ‐ ‐ Germination
3 + ‐ + Dormancy
4 ‐ ‐ ‐ Dormancy
5 ‐ ‐ + Dormancy
6 ‐ + ‐ Dormancy
7 ‐ + + Dormancy
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EMBRYO DORMANCY
A dormant embryo is characterized by
a high ABA/GA ratio, high ABA
sensitivity and low GA sensitivity.
Dormancy release involves degradation
towards a low ABA/GA ratio, a
decrease in ABA sensitivity and an
increase in GA sensitivity.
Thus, ABA dominates the embryo
dormancy program, and GA the
embryo germination program.
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COAT DORMANCY
The combination of an embryo with low
growth potential and mechanical constraint
from the seed covering layers can result in
coat dormancy.
GA can release this coat dormancy by
increasing the embryo growth potential
and/or by reducing the mechanical
constraint.
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TESTAAND ENDOSPERM DORMANCY
(1) Testa dormancy: ABA during seed
development determines GA requirement for
germination since ABA influences the testa
thickness and GA embryo growth potential.
2) Endosperm dormancy: Endosperm
weakening can be either part of the coat
dormancy release or part of the germination
program.
GA acts by increasing the embryo growth
potential and by promoting endosperm
weakening which is achieved through ABA-
independent and ABA-inhibited mechanisms.
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INDUCTION, MAINTENANCE AND RELEASE OF
PHYSIOLOGICAL DORMANCY BY HORMONES
ABA is an important positive regulator of both induction
and maintenance of dormant state in imbibed seeds
(Kucera et al., 2005, Finch-Savage and Leubner-
Metzger, 2006).
ABA-deficiency during seed development is associated
with absence of primary dormancy , whereas over-
expression of ABA biosynthesis can increase ABA
content and enhance dormancy
ABA synthesis in embryo and endosperm both seem to
contribute to induction of dormancy.
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MAINTENANCE(Contd…..)
de novo ABA biosynthesis during
imbibition of dormant, but not non-
dormant, seeds was demonstrated in
A. thaliana ecotype Cvi, as well as in
Nicotiana plumbaginifolia, Helianthus
annuus, and Hordeum vulgare (Finch-
Savage and Leubner-Metzger, 2006).
This de novo ABA biosynthesis is
interpreted as mechanism for
dormancy maintenance.
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RELEASE (Contd….)
Ambient environmental factors (e.g.
temperature) affect ABA/GA balance and
sensitivity to these hormones.
ABA synthesis and signalling (GA catabolism)
dominates dormant state, whereas, GA synthesis
and signalling (ABA catabolism) dominates
transition to germination.
The complex interplay between hormone
synthesis, degradation and sensitivities in
response to ambient environmental conditions
can result in dormancy cycling.
Change in the depth of dormancy alters the
requirements for germination (sensitivity to the
germination environment); when these overlap
with changing ambient conditions, germination
will proceed to completion.
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REGULATION OF DORMANCY AND GERMINATION BY ABA & GA
IN RESPONSE TO THE ENVIRONMENT (A. thaliana)
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Hormonal interactions during regulation of dormancy release
and germination of Nicotiana (a) and Brassica (b)
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(a) Nicotiana seed is two-step germination :
testa rupture followed by endosperm rupture.
Dormancy release and germination promotion
occur during seed after-ripening or via the
light-GA pathway during imbibition.
ABA inhibits endosperm rupture, but not testa
rupture.
GA, ethylene and BRs promote endosperm
rupture and counteract the inhibitory effects
of ABA.
ABA-inhibited class I β-1,3-glucanase genes
(βGlu I) which are transcriptionally induced
in the micropylar endosperm just before
endosperm rupture (Leubner-Metzger, 2003).
This, induction is highly localized in the
micropylar endosperm at the site of radicle
emergence.
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Light, GA and ethylene promote and ABA, osmotica
and darkness inhibit βGlu I expression and
endosperm rupture.
βGlu I is therefore, involved in endosperm rupture.
EREBP, ethylene-responsive element binding
protein transcription factor.
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(b) Brassica seed is one-step germination
No endosperm and so testa rupture plus
initial radicle elongation result in completion
of germination.
ABA does not inhibit testa rupture, but
inhibits subsequent radicle growth (Schopfer
& Plachy, 1984; Kucera et al., 2005).
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BR and light/GA promote endosperm rupture by
distinct signal transduction pathways.
GA and BR act in parallel to promote cell
elongation and germination and to counteract the
inhibitory action of ABA.
Cytokinins promotes cell division
Auxins have a major role in elongation
Mechanism of dormancy release & germination
17. 1 Reception 2 Transduction 3 Response
CYTOPLASM
PLASMA
MEMBRANE
Phytochrome
activated
by light
Cell
wall
Light
cGMP
Second messenger
produced
Specific
protein
kinase 1
activated
Transcription
factor 1 NUCLEUS
P
P
Transcription
Translation
De-etiolation
(greening)
response
proteins
Ca2+
Ca2+ channel
opened
Specific
protein
kinase 2
activated
Transcription
factor 2
An example of signal transduction pathway
1 The light signal is
detected by the
phytochrome receptor,
which then activates
at least two signal
transduction pathways.
2 One pathway uses cGMP as a
second messenger that activates
a specific protein kinase.The other
pathway involves an increase in
cytoplasmic Ca2+ that activates
another specific protein kinase.
3 Both pathways
lead to expression
of genes for proteins
that function in the
de-etiolation
(greening) response.