Aging is a highly complex process involving the cessation of chloroplasts, the decay mechanism of photosynthesis and the degradation of macromolecules like lipids, protein and nucleic acids (
Buchanan-Wollaston et al., 2005). The first visible event during aging so far is that the leaves turn yellow, which usually begins at the leaf edge advances to the blade
(Quirino et al., 2000). Integrated response of leaf cells namely leaf senescence provides information about age and many other external and internal signals (
Yoshida, 2003). This comprehensive aging retort offers an optimum adaptation to plants by fine-tuning the onset time, rate of progression and the nature of leaf senescence by incorporating the plant’s endogenous status into a given ecological environment (
Lim et al., 2007). There are various abiotic as well as biotic factors that are influencing leaf senescence
(Chen et al., 2002). To reproduce and survive under adversative situations, plants develop a variety of adaptive traits that are controlled by complex systems. Interconnected diverse networks operating in the downstream signaling cascade are regulated by transcriptional factors combined with cis elements present in their promoters. The knocking out genes relation also has a significant role in the senescence of any plant’s organs, such as fruits, flowers as well as leaves (
Lin and Wu, 2014).
ERF is one of the chief transcriptional factors in plants that regulates many stresses and progressive response pathways
(Li et al., 2015; Licausi et al., 2013). Thus, in our present hypothesized review, we pointed-out to observe the genetic relationship of
AtERFs genes in regulations of cell death in
Arabidopsis. Given that, Programmed Cell Death (PCD) including the expression of hundreds of genes, whereby several transcription factors act as core elements for the regulatory network
(Guo et al., 2004). Using genome- wide analysis, several
Arabidopsis genes can be identified through encoding the transcription factors like up-regulation in leaves’ aging
(Balazadeh et al., 2008; Buchanan-Wollaston et al., 2005). There are only a few factors that are being demonstrated in involving the regulation of cell death, by evaluating the leaf senescence appearances of knocking of mutants and by identifying downstream target genes. In this review, we will focus on the manifold roles of
TFs during genetic relationships. We will also deliberate how the Transcription factors family gene (
ERF) regulates the cell’s death by different hormonal stress, environmental strain and their role in retrograde signaling. These emergent complexity needs to be discussed first to explore the commercialized plants and understand the controlled molecular mechanism involved in it. The present hypothesized object is to emphasize the latest advances in this field based on our knowledge to provide a comprehensive overview of the role of these family genes in the
Arabidopsis plant.
Transcriptional regulations of cells death
Age-related phenomenon namely the aging of plants is meticulously associated with the death of cells. Leaf aging ensures the recycling from aging leaves to young leaves. The primarily plant-specific TFs like ERFs possess around 139 and 122 ERF family genes in
Arabidopsis (
Yoshida, 2003;
Nakano et al., 2006). The number of ERFs in different plants species may be variable: barley-121
(Guo et al., 2016), brassica- 291
(Song et al., 2013), cassava-147
(Fan et al., 2016), cotton Genus-271 species
(Lei et al., 2016), Solanum-155
(Charfeddine et al., 2015) and Triticum-117
(Zhuang et al., 2008). The process of aging is heritably linked to the death of cells and involves the regulated expression of genes relating to the cells’ death
(Lim et al., 2007). Microarray studies have revealed that
Arabidopsis thaliana has shown dramatic alterations in the gene expression patterns during age-reliant senescence
(Wagstaff et al., 2009). During aging forward, regulation of age-related cell death has been confirmed in the
Arabidopsis. The transcription factor-like ORESARA1 initiates aging-linked cell death in the leaves of
Arabidopsis having 28 days of age. However, during senescence, the downregulation of miR164 causes the negative regulation of ORE1 expression by miR164
(Kim et al., 2009). Besides ORE1, leaf necrosis also occurs due to higher expression of the WRKY6 transcription factor gene (Robatzek and Somssich, 2002). WRKY6 activates the promoter of the senescence-induced receptor KINASE1, which is specifically induced during the cell death of the leaves (Fig 1 and 2). Likewise, overexpression of the AP3/PI (AtNAP)/ANAC029 gene encoding NAC family transcription factors results from premature aging. The NAC transcription factor ORE1 SISTER1/ANAC059 is a progressive director of aging (Guo and Gan, 2006;
Balazadeh et al., 2011).
Progression of cells death and genes expression
At present today, the various forms of plant programmed cell death are indisputable during the development and environmental interactions
(Wu et al., 2014), limited information is available about molecular regulatory mechanisms of these processes. Though during the plant life cycle, cell death will be induced in various circumstances, it is not clear to date whether a common mechanism controlling different PCD types. During reports citations, we have found that numerous genes encoding nucleases, including BFN1, CAN1 and RNS3 are involved in transcriptionally regulated genes during differentiation-induced cell death. Though BFN1 is a renowned leaf senescence gene which too plays a significant part in the breakdown of chromatin in the root crown cells
(Fendrych et al., 2014). CAN1 is a plasma membrane-bound nuclease relating to the Staphylococcus, whose expression was previously accompanied by the cell’s death (
Ito and Fukuda, 2002), but its actual role is still unclear. A few reports have revealed that the SAUL1 mutant is deficient in the expression of the E3 ubiquitin ligase gene. SAUL1 looks to has miscalculated evolving age and turn on the adjustment switch for age-related cells seedling death (Fig 1). Though, in wild-type
Arabidopsis; the age-related involves miR164, ORE1 and EIN2 which ensure that the aging initiates the cells death in leaves. Throughout the leaf development, ORE1 accumulation is achieved by the downregulation miR164 that involve in the ethylene signaling leaf senescence
(Bisson et al., 2009). Moreover, ORE1 accumulates and SAG12 expression is usually prompted and age-related aging and cell-associated death can be noticed hastily Thus SAUL1 prevents cell death (under low light conditions) in the wild-type plants. Nonetheless, through genetic analysis, ORE1/ANAC092 in saul1-1/anac092-1 double mutant did not cause inhibition of the saul1 phenotype (Fig 1 and 2). The higher ORE1 expression itself is not adequate for causing the cells’ death and saul1 aging in plants
(Lesniewicz et al., 2012).
Senescence associated incidences and signaling
Premature senescence reduces the yield of annual crops while delaying senescence has a positive and negative impact on yield and nutritional quality. Genomic studies of leaf senescence-related to
Arabidopsis have been very efficacious in screening for mutants that have been impaired during senescence. The studies of influenced genes provide perceptions of the molecular basis of leaf senescence
(Liu et al., 2011). However, no obvious senescence phenotype was observed in most of the senescence-associated mutant genes (SAG) recognized by the reverse genetic approach
(Jing et al., 2005; Li et al., 2012). The expression of many senescence-associated genes (SAGs) is up-regulated during senescence, while the expression of photosynthesis-associated genes (PAGs) is down-regulated (Fig 1). Investigations on the SAGs have indicated a complex regulation of leaf senescence (
Nam, 1997;
Gan and Amasino, 1997). The age of individual leaf plays a significant role in determining the longevity of leaf in
Arabidopsis (Lim et al., 2007; Jing et al., 2002). Floral initiation can affect the longevity and senescence of plants
(Levey and Wingler, 2005;
Nooden and Penney, 2001). Certain to that, the findings also support accelerated and initiated leaf senescence, which is used to reduce chlorophyll content in silent plants
(Lim et al., 2007; Quirino et al., 2000; Hee et al., 2010). Besides, other family plant transcription factors usually have comparable roles. For example, the WRKY and NAC family genes are aging linked to well-known transcription (Fig 2). During the development of activated senescence in the
Arabidopsis, more than 20% of the 109 NAC family genes are explicitly tempted. Combining all these observations, the profile of transcription factor findings indicate that the cue agent can play a directing role in the initiation of cells death signs and leaf senescence singling, whereas using the transcriptional activation or inhibition of genes involved in the leaf development it can control the senescence (
Buchanan-Wollaston et al., 2005).
Functions of age-dependent associated Genes and network in cells death
Leaf senescence advances with age, where the process includes complex regulation of the premature life stages of the leaf as well as many exogenous and endogenous factors
(Buchanan-Wollaston et al., 2005). There are a lot of SA genes whose coordinated expression regulates the plant senescence. By identification and characterization of several SA genes and many aging concerned mutants, a major molecule breakthrough has been explored through this phenomenal understanding. The transcription genes function as a progressive regulator in the age of reliant leaf senescence. They interact with the
RGL1, however,
RGL1 impedes the transcriptional function of WRKY45 (Table 1). Moreover, several transcription factors are also prompted during the transcription stage, though combinable suggest the directing role of complex transcriptional regulatory networks in the leaf senescence
(Liu et al., 2011). It will be very interesting, in the forthcoming future, to identify the possible modifications in aging and aging correlated proteins, which will offer further understanding of leaf senescence and cell death mechanisms. Further, the leaf aging of any plant leads to the identification of thousands of SA genes
(He et al., 2001), while the utmost SA genes mutations modify the leaf senescence (Fig 1 and 2). It may be due to the functional termination aging process
(Li et al., 2012). At the same time, the forward genetics approach in
Arabidopsis has been determined in a group of leaf senescence concerned genes like ORE genes
(Lim et al., 2007; Jing et al., 2005; Woo et al., 2001) and death regulating genes of plant leaves (
Guo and Gan, 2006;
Kim et al., 2009). Presumed those molecular mechanisms of controlling plant senescence and cell death have wide-ranging prospects for improving crop yield potential and nutritional quality under optimal and stressful conditions. While, many
TFs families, particularly those from the NAC, WRKY and ERF families
(Guo et al., 2004; Breeze et al., 2011) exhibited an effect of modulating senescence. Reports suggested that different genes identified in the NAC transcription family
viz. ORE1, AtNAP, ORS1, ATAF1, NTL4, WRKY53 and WRKY22 to regulate the senescence and cell death in
Arabidopsis leaves (
Gregersen and Holm, 2007;
Miao et al., 2004) (Table 1).
Role of different hormones in regulation of cells death
It is reported that the regulation of phytohormones serves as an endogenous signal, including senescence and cell death almost in all prospectuses of plant growth and development. Abscisic acid (ABA), Auxin, Jasmonic Acid (JA), Ethylene, Cytokinin and Gibberellin (GA) play important roles in promoting or inhibiting aging dependent activities
(Cai et al., 2002; VanDoorn, 2008). Further, the significant effects of hormones on the regulation of cell death of plants are briefly described below:
Ethylene regulates the cell death
It has been reported that the regulation of ethylene serves as an endogenous signal including senescence in almost instructions for plant growth and development (
Chen, 2011;
Van Doorn, 2008). The aging is accompanied by a sudden and transient increase in respiration associated with increased ethylene production (
Xu and Hanson, 2000). In Dianthus, exposure to ethylene causes premature senescence of petals and increases or decreases the abundance of mRNA populations, suggesting that physiological changes in petals may be the result of rapid changes in gene expression
(Ahlfors et al., 2004; Huang et al., 2007). As earlier revealed that the ethylene is a necessary regulator of the cell death pathway triggered in the vad1-1. In contrast, in the mutant vad1-1 the degree of cell death was increased and in cells that overexpressed ERF1; a positive regulator of ethylene response and CTR1; a negative regulator of ethylene signaling; in the CTR1 mutant the death time consistently increased. In this regard, the use of ethylene accounts for the amplification of superoxide accumulation, thereby promoting the execution of diffusion cell death
(Overmyer et al., 2000).
Cytokinin induced cell death
Cytokinin (CKs) plays a significant role in cell division, proliferation and differentiation. It participates in several aspects of plant growth including seed sprouting, inhibit the yellowing, differentiation of chloroplast, apical supremacy, as well as aging of cells
(Argueso et al., 2009; Werner and Schmulling, 2009). It has been recently proved that a high level of CK induces programmed cell death (PCD) in the plant cells
(Carimi et al., 2003). 6-benzyl amino purine (BA) showed a high frequency of suspension cell culture of several plants including
Arabidopsis, carrot and alfalfa cells decreased growth and induced cell death
(Zottini et al., 2006).
Gibberellin (GA) signaling in leaf senescence
The gibberellin (GA) plays an elusive role in the signaling in leaf senescence. Various studies have shown that the influence of GA on leaf senescence depends on the GA dose and the condition of the treated leaf
(Chen et al., 2011). While this further requires clarification. Investigations have confirmed that the Gibberellin Insensitive Dwarf1 (GID1) GA receptor / Della repressor pathway receives and transduces the GA signal (
Sakakibara, 2006). Moreover, Della proteins such as Repressor OF ga1-3 (RGA), GA Insensitive (GAI), RGL2, RGA-LIKE 1 (RGL1) and RGL3, have unique overlapping functions and act as the main repressors of about all GA responses, in the Arabidopsis (
Mlejnek and Prochazka, 2002).
