Agriculture Reference
In-Depth Information
sulu et al.
2007
). Despite this, there are some aspects of the plant stress response
which still need to be explored.
This chapter will focus on the effects of oxidative stress within the nuclear com-
partment where DNA becomes the main target of the highly toxic reactive oxy-
gen species (ROS). Several abiotic stresses (e.g., water deficit, high salt, UV-light,
ionizing radiation, heavy metals, and ozone) can trigger DNA damage by directly
acting on the double helix structure or by enhancing the intracellular ROS levels
(Tuteja et al.
2009
). Oxidative DNA damage requires prompt repair to maintain
genome integrity and preserve the fidelity of genetic information. The response of
plant cells to genotoxic stress relies on the activity of multiple DNA repair pathways
which share some common elements with animal cells, but also own distinctive
features, unique to the plant kingdom.
This chapter will cover the recent advances in the field of plant DNA repair,
highlighting novel gene functions directly involved in the response mechanism to
abiotic stresses, not only at the plant level but also in seeds. As for the molecular
mechanisms involved in the regulation of DNA repair, some intriguing findings
that link the genotoxic stress response to complex cellular networks, e.g., the small
regulatory Ribonucleic acids (RNAs) and the circadian clock, are reported.
2 Genotoxic Stress: Effects Inside and Outside the Nucleus
Differently from animal systems where genotoxic agents are mainly investigated
as a major cause of human cancer (Evans et al.
2004
), genotoxic stress in plants
is essentially considered as a critical factor which impairs fitness and productivity
by affecting genome stability (Tuteja et al.
2009
; Roldan-Arjona and Ariza
2009
).
The most frequent DNA lesions are oxidative base damage, alkylation, deam-
ination, abasic (apurinic and/or apyrimidinic, AP) sites and single-strand breaks
(SSBs; Tuteja et al.
2009
). Accumulation of 7,8-dihydro-8-oxoguanine (8-oxo-dG),
the most common oxidized base lesion formed
in vivo
in animal cells, has been
investigated also in plants (Balestrazzi et al.
2009
,
2011a
) and cell suspension cul-
tures (Balestrazzi et al.
2010
) challenged with different abiotic stresses. Other DNA
lesions, e.g., UV-photoproducts and bulky chemical adducts, dramatically alter the
DNA structure (Tuteja et al.
2009
; Roldan-Arjona and Ariza
2009
). Perception of
genotoxic stress and the activation of signal transduction lead to cell cycle arrest
and this allows the regulated expression of DNA repair genes.
Several genotoxic agents can simultaneously cause both DNA damage within the
nucleus and oxidative stress outside the nuclear compartment, leading to complex
molecular activity which might ultimately result in programmed cell death (PCD).
Besides the enhancement of DNA repair, antioxidant mechanisms are activated in-
side and outside the nuclear compartment. There is evidence to demonstrate that
the control of the nuclear thiol-disulfide redox state is dependent on reductant mol-
ecules such as glutathione and thioredoxin, as well as on the presence of specific
isoforms of antioxidant enzymes. All these nucleus-specific pathways are distinct
