Plants are prone to a number of biotic stress conditions. The suite of molecular and cellular processes is triggered once the plant senses stress (Rejeb et al., 2014; Lamers et al., 2020), which in turn activates a cross-wired mesh of morphological, physiological, and biochemical mechanisms (Nejat and Mantri, 2017; Saijo and Loo, 2020). Plants have developed complex sensory mechanisms to identify biotic invasion and overcome the detriment of growth, yield, and survival (Rizhsky et al., 2004; Lamers et al., 2020). Consequently, plants have evolved a surfeit of responses to defend themselves against attacks by a broad spectrum of pests and pathogens, including viruses, nematodes, bacteria, fungi, and herbivorous insects (Hammond-Kosack and Jones, 2000). Thus, plants tend to strike a balance between their response and biotic stress to combat the deleterious effect on their survival (Peck and Mittler, 2020). The molecular mechanisms contributing toward plant defense responses had been elucidated to a great depth (Cheng et al., 2012; Wang Z. et al., 2019). But how and why different signaling pathways converge to biotic stress responses still remain obscure. The light signaling pathway is one such area of interest amongst the research community.

Dark and light alterations are fundamental to plant survival. It affects all aspects of plant growth and development. The light signals are perceived by photoreceptors, which are capable of discriminating various wavelengths of light (Franklin et al., 2004). Photoreceptors, namely, phytochromes (sense red and far-red light), phototropins, and cryptochromes (sense blue light and UV light), develop cues from qualitative and quantitative light alterations (Christie, 2007; Yu et al., 2010; Tilbrook et al., 2013). This sensing activates several signal transduction pathways, which in turn regulate plant growth, physiology, morphology, and immunity (Kami et al., 2010; Moreno and Ballaré, 2014; Mawphlang and Kharshiing, 2017; Tripathi et al., 2019). In addition, photosynthetic reactions themselves regulate biochemical machinery in plant tissues (Lu and Yao, 2018). This is evident by the point that a number of genes are transcriptionally induced by the circadian clock in Arabidopsis thaliana and other plants (Harmer et al., 2000; Creux and Harmer, 2019). Circadian clock has been reported to meticulously regulate the defense machinery in plants (Sharma and Bhatt, 2015).

There are two developmental fates of seedling upon germination that are primarily dependent upon the presence or absence of light. In the presence of light, seedlings develop a shorter hypocotyl and open green cotyledons. This default pathway of plant development is termed photomorphogenesis (Bae and Choi, 2008; Pham et al., 2018). On the contrary, plants grown in dark conditions undergoes skotomorphogenesis (plant development under dark conditions), allocating the resources toward hypocotyl elongation rather than on cotyledon or root development (Josse and Halliday, 2008). Elongated hypocotyls, closed cotyledons, and an apical hook at the shoot meristem are characteristic to skotomorphogenetic plant development (Pham et al., 2018). Skotomorphogenesis is accomplished by repressing genes implicated in de-etiolation and photomorphogenic development (Josse and Halliday, 2008). Additionally, the effect of dark/light alteration is not only limited to plant growth and development, but it also impacts other responses to the environment such as defense against pests and pathogens (Ballaré, 2014). Extensive research exists to vindicate the effect of dark/light alterations on plant defense responses, extending from biological to ecological scales (Huner et al., 1998; Roberts and Paul, 2006; Kazan and Manners, 2011; Ballare et al., 2012; Kangasjärvi et al., 2012; Hua, 2013; Garcia-Guzman and Heil, 2014; Saijo and Loo, 2020). But the in-depth mechanistic details with regard to the complex regulatory networks are yet to be explored. The basic research in this direction can assist the idea of sustainable agriculture to ensure food security for the ever-growing world population (Sánchez-Muros et al., 2014; González de Molina et al., 2017; Iqbal et al., 2020a; Saiz-Rubio and Rovira-Más, 2020). The present review recapitulates biochemical, physiological, and molecular aspects of biotic stress and plant defense responses operating in light/dark scenarios.

A number of pests, parasites, and pathogens are responsible for infecting plants and inciting biotic stress. Fungal parasites can be either necrotrophic (kill host cell by toxin secretion) or biotrophic (feed on living host cell). They are capable of inducing vascular wilts, leaf spots, and cankers in plants (Laluk and Mengiste, 2010; Doughari, 2015; Sobiczewski et al., 2017). Nematodes feed on plant parts and primarily cause soil-borne diseases leading to nutrient deficiency, stunted growth, and wilting (Lambert and Bekal, 2002; Bernard et al., 2017; Osman et al., 2020). Similarly, viruses are also capable of local and systemic damage resulting in chlorosis and stunting (Pallas and García, 2011). On the contrary, mites and insects impair plants by either feeding (piercing and sucking) on them or laying eggs. The insects might also act as carriers of other viruses and bacteria (Schumann and D’Arcy, 2006). Plants have developed an elaborate immune system to combat such stresses (Taiz and Zeiger, 2006; Saijo and Loo, 2020). Plants have a passive first line of defense, which includes physical barriers such as cuticles, wax, and trichomes to avert pathogens and insects. Plants are also capable of producing chemical compounds to defend themselves from infecting pathogens (Taiz and Zeiger, 2006) (discussed in section “Effect of Dark/Light on Plant–Pathogen Interaction and Associated Mechanisms”). Additionally, plants trigger defense against biotic agents by two levels of pathogen recognition (Dangl and McDowell, 2006).

The first level of pathogen recognition encompasses pattern recognition receptors (PRRs), which identify pathogen-associated molecular patterns (PAMPs). Such plant immunity is categorized as PAMP-triggered immunity (PTI) (Monaghan and Zipfel, 2012). Phytophagous pests respond by identification of herbivore-associated elicitors (HAEs), herbivore-associated molecular patterns (HAMPs), or PRR herbivore effectors (Santamaria et al., 2013). The second level of pathogen recognition encircles plant resistance (R) proteins, which identify specific receptors from a pathogen (Avr proteins) (Dangl and McDowell, 2006; Gouveia et al., 2017; Abdul Malik et al., 2020). It is considered an effective mechanism of plant resistance to pests and involves effector-triggered immunity (ETI) (Kaloshian, 2004; Mur et al., 2008; Spoel and Dong, 2012). ETI stimulates hypersensitive responses (HRs) and triggers programmed cell death (PCD) in infected and surrounding cells (Mur et al., 2008). The proteins encoded by a majority of R genes have a specific domain with conserved nucleotide-binding site (NBS). The second next important domain is leucine-rich repeat (LRR). Pathogen effectors are recognized directly (physical association) or indirectly (association of an accessory protein) by NB-LRR receptors (Dodds and Rathjen, 2010). Sometimes, R gene-mediated plant response toward invading pathogen provokes a higher degree of defense, termed as systemic acquired resistance (SAR). SAR generates whole-plant systemic resistance against a broad spectrum of pathogens. In SAR, a local encounter results in the stimulation of resistance to the other plant organs through intraplant communication (Fu and Dong, 2013). Generally, both categories of plant immune responses induce the same reaction, but ETI is considered more rigorous to pathogen infection (Tao et al., 2003).

Perturbations in cytosolic calcium (Ca²⁺) concentrations are the earliest signaling events occurring upon the exposure of plants to biotic stress. Ca²⁺ signals are the center to plant immune signaling pathways (Seybold et al., 2014; Aldon et al., 2018). Rapid and transient perturbations in Ca²⁺ concentrations are crucial to gene reprogramming required to generate an adequate response (Reddy et al., 2011). The plant immune responses differ in their Ca²⁺ signatures. For example, Ca²⁺ transients upon PTI activation returns to basic levels within a few minutes (Lecourieux et al., 2005), while ETI involves a prolonged increase in cytosolic Ca²⁺ levels lasting for several hours (Grant et al., 2000). Lanthanum, a known Ca²⁺ channel blocker, is reported to hinder the immune responses associated with both PTI and ETI (Grant et al., 2000; Boudsocq et al., 2010). Precisely, in response to the biotic invasion, PTI and ETI activate the Ca²⁺ ion channels, resulting in an increase of cytoplasmic Ca²⁺ concentrations (Figure 1). In A. thaliana, cyclic nucleotide-gated channels (CNGCs), glutamate receptor-like channels (GLRs), stretch-activated Ca²⁺ channels (OSCAs), and the MID1-complementing activity (MCA) families are the four main plasma membrane Ca²⁺-permeable channels (Dodd et al., 2010; Yuan et al., 2014; Liu et al., 2018). Twenty distinct members of the CNGC family of plasma membrane Ca²⁺-permeable channels have been identified in A. thaliana (Meena and Vadassery, 2015; DeFalco et al., 2016). CNGCs are extensively linked to plant development and biotic stress responses (Meena and Vadassery, 2015; DeFalco et al., 2016; Breeze, 2019). In response to fungal and bacterial pathogens, the Ca²⁺-permeable channels CNGC2, CNGC4, CNGC11, and CNGC12 are reported to play critical roles in the entry of Ca²⁺ ions inside the plant cell (Yoshioka et al., 2001; Ahn, 2007). The role of CNGC2, CNGC4 (Ma et al., 2012; Chin et al., 2013), CNGC11, and CNGC12 (Yoshioka et al., 2006; Moeder et al., 2011) has been well established in plant immune responses. Very recently, the function of CNGC19 Ca²⁺ channel was also extended to herbivory-induced Ca²⁺ flux, plant defense responses against pathogen Spodoptera litura (Meena et al., 2019), and basal defense signaling to regulate colonization of Piriformospora indica on A. thaliana roots (Jogawat et al., 2020). The first CNGC from plants was identified nearly two decades ago in barley as a calmodulin (CaM)-binding protein (Schuurink et al., 1998). CNGCs from plants and animals are reported to possess one or more CaM-binding domains at their cytosolic N- and C-termini, but the gating of CNGCs from plants is not well deduced (DeFalco et al., 2016; Fischer et al., 2017; James and Zagotta, 2018). The progress of plant CNGC research has been relatively low due to the difficulties in electrophysiological studies encircling CNGCs. However, the recent technological advances and reliability on reverse genetics using cngc mutants have resulted in few successful studies (Gao et al., 2016; Chiasson et al., 2017; Wang et al., 2017; Zhang et al., 2017). CNGC7, CNGC8, and CNGC18 have been specifically reported to act together with CaM2 as a molecular switch that operates in response to cellular Ca²⁺ concentrations (Pan et al., 2019). Additionally, CNGC18 is co-expressed with CPK32, indicating the regulation of its activity by phosphorylation (Zhou et al., 2014). Similarly, GLRs, which are systematically classified into three clades—clade I (GLRs 1.1–1.4), clade II (GLRs 2.1–2.9), and clade III (GLRs 3.1–3.7) (Lacombe et al., 2001)—are linked to plant defense against Botrytis cinerea (Sun et al., 2019) and Hyaloperonospora arabidopsidis (Manzoor et al., 2013). As such, the role of AtGLR3.3 and AtGLR3.6 in aphid-elicited cytosolic Ca²⁺ elevation is also well established (Vincent et al., 2017). In-vitro kinase assay confirmed that AtGLR3.7 is phosphorylated by CDPK3, CDPK16, and CDPK34 at serine-860 site (Wang P.-H. et al., 2019). CDPKs have been extensively associated with plant stress management and development (Singh et al., 2017). The other plasma membrane localized Ca²⁺-permeable channels, namely, OSCAs (phosphorylation of OSCA1.3 by BIK1) and MCAs (MCA1 and MCA2), are reported to regulate plant stomatal immunity (Thor et al., 2020) and manage hypergravity in A. thaliana hypocotyls under dark conditions, respectively (Hattori et al., 2020). Apart from the Ca²⁺ channels localized in the plasma membrane, several other Ca²⁺ channels are known to exist in the endoplasmic reticulum, mitochondria, golgi body, and plant vacuole (Singh et al., 2014; Xu et al., 2015a; Costa et al., 2018; Pandey and Sanyal, 2021). For example, autoinhibited Ca²⁺-ATPases (ACAs), ER-type Ca²⁺-ATPases (ECAs), mitochondrial Ca²⁺ uniporter (MCU), P1-ATPases (e.g., HMA1), Ca²⁺ exchangers (CAX), two-pore channel (TPC), 1,4,5-trisphosphate receptor-like channel (InsP₃R), 1,4,5-trisphosphate (IP₃), cyclic ADP-ribose (cADPR)-activator ryanodine receptor-like channel (RyR), slow-activating vacuolar channel (SV), and sodium-calcium exchanger (NCX) represents the organellar Ca²⁺ machinery (Figure 1). Many of these channels are reported to play pivotal roles in plant immunity (Bose et al., 2011; Pittman, 2011; Spalding and Harper, 2011; Kiep et al., 2015; Costa et al., 2017; Teardo et al., 2017; Yang et al., 2017; Demidchik et al., 2018; Taneja and Upadhyay, 2018; Pandey and Sanyal, 2021).

Once the Ca²⁺ ion enters the cell, it is sensed by an array of Ca²⁺-binding proteins. The Ca²⁺-binding proteins work as Ca²⁺ sensors decoding complex Ca²⁺ signatures (Kudla et al., 2018). Ca²⁺ sensors are highly conserved proteins and are classified into (a) CaM and CaM-like proteins (CMLs), (b) calcineurin-B-like proteins (CBLs), and (c) Ca²⁺-dependent protein kinases (CPKs) and Ca²⁺ and Ca²⁺/CaM-dependent protein kinase (CCaMK) (Cheng et al., 2002; Luan, 2009; Bender and Snedden, 2013; Ranty et al., 2016). CaM, CMLs, CBLs, and CPKs are comprehensively involved in the cross-talk of various biotic and abiotic stress signals (Ranty et al., 2016; Aldon et al., 2018). Many Ca²⁺ and Ca²⁺ sensor-associated transcription factors (TFs) are implicated in stress signaling in plants (Carrion et al., 1999; Singh and Virdi, 2013; Ranty et al., 2016; Chung et al., 2020; Shen et al., 2020). The largest and best characterized family of Ca²⁺/CaM-dependent TFs are CAMTAs (Iqbal et al., 2020b). CAMTA3 has been reported enormously as a suppressor of plant biotic defense responses (Benn et al., 2016; Jacob et al., 2018; Kim et al., 2020). It works downstream to MAP kinase (Bjornson et al., 2014) and is directly phosphorylated and degraded by flg22-responsive mitogen-activated protein kinases (MAPKs) (Jiang et al., 2020). Precisely, MPK3 and MPK6 activate CAMTA3 nuclear export and destabilization (Jiang et al., 2020). Similarly, NAC TF, upon interaction with Ca²⁺/CaM, positively regulates various biotic stress responses in Solanum lycopersicum (Wang G. et al., 2016). NAC is also responsive to Colletotrichum gloeosporioides and Ralstonia solanacearum infection in woodland strawberry (Zhang et al., 2018). WRKY is another Ca²⁺/CaM-dependent TF (Park et al., 2005; Yan et al., 2018) implicated in pathogen incursion (Park et al., 2005; Bai et al., 2018). WRKY7, WRKY45, WRKY43, WRKY53, and WRKY50 in a Ca²⁺-driven manner bind to various isoforms of CaM (Park et al., 2005; Popescu et al., 2007). MYB TF is also well characterized as a Ca²⁺-dependent TF. MYB functions upstream in a vast majority of defense-responsive and abiotic stress-receptive genes (Stracke et al., 2001; Chezem et al., 2017; Li et al., 2019). Similarly taking CMLs into consideration, AtCML9 works as positive regulator of plant immune response. It was found to be induced by Pseudomonas syringae and phytohormones including abscisic acid (ABA) and salicylic acid (SA) (Magnan et al., 2008; Leba et al., 2012). Further, AtCML9 interacts with WRKY53 and TGA3 TFs, both of which are known to mediate biotic stress responses (Popescu et al., 2007). In concurrence, AtCML37 and AtCML42 are associated with defense against herbivorous insects (Spodoptera littoralis) (Vadassery et al., 2012; Scholz et al., 2014). Very recently, 17 AcoCPK genes from Ananas comosus (pineapple) were analyzed for their effect under biotic stress. AcoCPK1, AcoCPK3, and AcoCPK6 were shown to render susceptible disease resistance in A. thaliana against Sclerotinia sclerotiorum (Zhang et al., 2020). Another class of Ca²⁺ sensors, CBLs, are known to specifically interact with a family of plant-specific CBL-interacting protein kinases (CIPKs). CBL interacts with Ca²⁺ and binds with CIPK, resulting in kinase activation. The CBL–CIPK complex actively regulates downstream target proteins by phosphorylation (reviewed by Ma et al., 2020; Tang et al., 2020).

The other initial responses of pathogen attack on plants include the generation of reactive oxygen species (ROS) and activation of mitogen-activated protein kinases (MAPKs) (Muthamilarasan and Prasad, 2013). ROS and MAPKs overlap with other signaling pathways, including light pathways (Goldsmith and Bell-Pedersen, 2013; Foyer, 2018). Furthermore, pest attack on plants activates local or systemic defense responses involving oligogalacturonoids (OGAs), jasmonic acid (JA), and hydrogen peroxide (H₂O₂) signaling pathways (Fürstenberg-Hägg et al., 2013). Plants are also capable of producing volatile compounds that repel attacking pests (discussed in section “Effect of Dark/Light on Plant–Pathogen Interaction and Associated Mechanisms”). These compounds are part of lipoxygenase (LOX) and terpenoid signaling pathways (Pichersky and Gershenzon, 2002; Dudareva et al., 2006). Another pivotal downstream defense mechanism by plants include the generation of defensive proteins and universal stress proteins. These proteins comprise protein inhibitors, lectins, chitinases, α-amylase inhibitors, and polyphenol oxidases (Fürstenberg-Hägg et al., 2013; Lee et al., 2019). Additionally, the role of pathogenesis-related (PR) genes in plant defense responses has been considerably explored (Ali et al., 2018). PR genes translate into proteins that are induced in plants only upon pathological or similar conditions (conditions of non-pathogenic origin) (Jain and Khurana, 2018). They are considered as an important component of plant innate immune response and are implicated in HR and SAR responses (Jain and Khurana, 2018). PR proteins are grouped into 17 families, depending upon their biochemical and molecular properties (van Loon et al., 2006). In A. thaliana, five PR genes (PR-1, PR-2, PR-3, PR-4, and PR-5) are routinely explored for their involvement in plant biotic interactions (Hamamouch et al., 2011). PR-1, PR-2, and PR-5 are implicated in SA-dependent SAR response, while PR-3 and PR-4 are involved in JA-dependent SAR response (Thomma et al., 1998; Hamamouch et al., 2011). An important aspect associated with PR proteins is their simultaneous indulgence in biotic and abiotic stress (Ali et al., 2018). To substantiate this, the 1,000-bp upstream region of all five PR genes from A. thaliana were analyzed bioinformatically to determine the presence of different motifs associated with a variety of environmental stresses. Intriguingly, all the PR genes contained multiple light-responsive motifs (AE-box, GAP-box, GT-1 motif, G-box, GATA-motif, box-4, and chs-CMA2a). The presence of light-responsive motifs in the promoter region of PR genes probably implies the binding of light-dependent genes to these conserved sequences (Figure 2). This notion itself supports the idea of intense cross-talks between biotic stress responses and light signaling pathways.

Finally, the involvement of phytohormones in regulating plant biotic defense responses cannot be ruled out. ETI and PTI induces specific downstream signaling pathways, in which three phytohormones are crucial, namely, SA, JA, and ethylene (ET). SA regulatory pathways are responsive to biotrophic and hemi-biotrophic pathogenic agents. Similarly, JA and ET pathways are responsive to necrotrophic agents and chewing pests (Bari and Jones, 2009; De Vleesschauwer et al., 2014). SA stimulates the SAR pathway promoting the expression of PR genes, which in-turn renders tolerance against a wide range of pathogens (Grant and Lamb, 2006; Fu and Dong, 2013; Ádám et al., 2018). SA, JA, and ET regulatory pathways for plant defense exhibit significant divergence, but they overlap to render defense against pathogenic agents (Glazebrook, 2005; Ku et al., 2018). Additionally, ABA, auxin, brassinosteroids (BRs), cytokinin (CK), gibberellic acid (GA), and peptide hormones also have vital significance in regulating the immune responses of the plants (Bari and Jones, 2009; Ku et al., 2018; Islam et al., 2019; Chen et al., 2020). Amongst all the phytohormones, JA is critical in triggering the plant defense system and cross-talks with other phytohormonal pathways to stimulate the plant immune responses (Yang et al., 2019).

Plants are exposed to variable light intensities that encompass light perception and signaling pathways responsible for growth, development, and immune responses (Hua, 2013; Ballaré, 2014). Nevertheless, plants often confront light intensities that exceed their photosynthetic capacity, inducing light stress (Mishra et al., 2012). Mechanisms encompassing light/dark alteration under stress conditions have been comprehensively studied (Mittler, 2002; Cerdán and Chory, 2003; Jiao et al., 2007; Koussevitzky et al., 2007; Mühlenbock et al., 2008; Alabadí and Blázquez, 2009; Chory, 2010; Kami et al., 2010; Lau and Deng, 2010; Trotta et al., 2014; Kaiserli et al., 2015; Saijo and Loo, 2020). Given the extreme importance of light for survival, immunity, growth, and development, plants have evolved the capability to sense and respond to different spectra of light (visible, infrared, ultraviolet, etc.) through photoreceptors. In A. thaliana, five distinctive genes (PHYA–PHYE) encode phytochrome protein (Clack et al., 1994; Li et al., 2011). They potentially act as receptors for red and far-red lights (Takano et al., 2009). Similarly, in A. thaliana, cryptochromes encoded by CRY1 and CRY2 dedicatedly sense blue (∼400 nm) and green (500–600 nm) lights and UV-A (Folta and Maruhnich, 2007; Jiao et al., 2007; Bae and Choi, 2008; Jenkins, 2009).

As previously discussed, plants undergo skotomorphogenesis in the absence of light while photomorphogenesis in the presence of light (see section “Introduction”). Repressor proteins such as constitutive photomorphogenic/de-etiolated1/fusca (COP/DET/FUS) inhibit photomorphogenesis under dark conditions (Hardtke and Deng, 2000; Dong et al., 2014). Mutants with defects in any of these repressor proteins display constitutive photomorphogenic (COP) phenotypes under dark conditions (Lau and Deng, 2012). The repressor proteins are characterized into four categories with overlapping functions and have been studied extensively (Deepika et al., 2020; Pham et al., 2020). The first one is COP1, which is a RING-finger-type ubiquitin E3 ligase (Deng et al., 1992). Under dark conditions, it acts as a repressor of light signaling and accumulates in the nucleus (Xu D. et al., 2014). On the contrary, COP1 is exported out of the nucleus, facilitating photomorphogenesis under light conditions (von Arnim et al., 1997; Hardtke et al., 2000; Seo et al., 2003; Duek et al., 2004; Xu et al., 2016a; Podolec and Ulm, 2018). COP1 acts as a central repressor and facilitates ubiquitination and degradation of various positive regulators of light, namely, long hypocotyl in far-red 1 (HFR1), long hypocotyl 5 (HY5), and long after far-red light 1 (LAF1) (Hardtke et al., 2000; Osterlund et al., 2000; Jang et al., 2005; Yang et al., 2005). The degradation of positive regulators of light by COP1 is constrained under light by prohibiting COP1 protein from the nucleus. This triggers the initiation event of photomorphogenesis. The function of COP1 has been extensively linked to light signaling (Figure 2). However, it is also implicated in the regulation of flowering time, circadian rhythm, and temperature signaling (Ma et al., 2002; Yu et al., 2008; Jeong et al., 2010; Catalá et al., 2011; Menon et al., 2016; Wang W.-X. et al., 2016; Xu et al., 2016b; Hoecker, 2017). COP1 is also known to interact with the suppressor of PHYA 1–4 (SPA 1–4). This interaction results in tetrameric complexes comprising two COP1 and two SPA proteins (COP1/SPA complex) (Zhu et al., 2008). SPA proteins are reported to positively enhance COP1 function (Ordoñez-Herrera et al., 2015). Skotomorphogenesis is accomplished by suppressing the expression of genes involved in photomorphogenic development in the dark (Josse and Halliday, 2008). This is tightly regulated by the COP1–SPA1E3 ligase complex (Osterlund et al., 2000; Josse and Halliday, 2008; Ordoñez-Herrera et al., 2015; Holtkotte et al., 2016; Paik et al., 2019). COP1–SPA1E3 ligase targets HY5 TF for degradation by the proteasome (Osterlund et al., 2000). COP1–SPA complex interacts with CULLIN4 (CUL4) to form CUL4–COP1–SPA complex. CUL4–COP1–SPA complex acts as CULLIN ring E3 ligase (CRL) and degrades positively acting TFs under dark conditions to suppress photomorphogenesis (Chen et al., 2010). Interestingly, CUL4–COP1–SPA complex has a dual function in dark/light-induced photomorphogenesis (Zhu et al., 2015; Paik et al., 2019). CUL4–COP1–SPA complex activates early ubiquitin-mediated degradation of phytochrome interacting factor 1 (PIF1) to trigger light-induced seed germination (Zhu et al., 2015; Paik et al., 2019). The second group of repressor protein is COP9 signalosome (CSN). It is highly conserved and comprises eight subunits (Serino and Deng, 2003). CSN had been reported to be implicated in deneddylation/derubylation of CRLs (Schwechheimer et al., 2001). The third group of repressor protein is de-etiolated1 (DET1), COP10, DNA damage-binding protein 1 (DDB1), and CUL4. DET1 is known to bind histone H2B (Benvenuto et al., 2002). It also regulates PIFs and HFRs to suppress seed germination and photomorphogenesis under dark conditions (Dong et al., 2014; Shi et al., 2015). Finally, the fourth group of repressor protein is PIFs (PIF1–PIF8) that belong to basic helix-loop-helix (bHLH) family of TFs and suppresses photomorphogenesis under dark conditions (Leivar et al., 2008; Shin et al., 2009; Leivar and Quail, 2011; Pham et al., 2018). They bind to the G-box consensus sequence in the 1,000-bp upstream region of light-responsive genes. Under dark conditions, phytochromes physically interact with PIFs to repress light response. The activation of photoreceptors suppresses COP1/SPA E3 ubiquitin ligase complexes and PIFs (Martínez et al., 2018b). This eventually activates HY5 to modulate the expression of light-inducible genes and disrupts PIF function (Chen et al., 2013; Toledo-Ortiz et al., 2014; Gangappa and Kumar, 2017). Upon plant exposure to dark conditions, photoreceptor inactivation enables COP1/SPA- and PIF-mediated disruption of light signaling (Xu X. et al., 2014; Xu et al., 2015b, 2017). This signaling cascade promotes plant growth by involving phyto-hormones (such as BR, auxins, and GA) at the cost of plant immunity (Lozano-Durán and Zipfel, 2015; Martínez et al., 2018b).

Photoreceptors are also responsible to determine the quality of light (R:FR ratios). Upon excitation by R light, phytochromes are transformed into FR light-absorbing state (biologically active “Pfr”). Since red light is absorbed by chlorophyll and carotenoids, its quantity is significantly decreased when penetrating through a dense canopy (Slattery et al., 2017; Walker et al., 2018). Shade-intolerant plants (such as A. thaliana) perceive and respond to such conditions by elongating stems and promoting flowering (Fiorucci and Fankhauser, 2017). This is an evolutionary phenomenon developed in plants and is termed shade-avoidance syndrome (SAS). Plants exhibit SAS, which is represented by the elongation of plant parts such as hypocotyls, stems, and petioles (Casal, 2013). Both PHYA and PHYB proteins contribute towards SAS. PHYB restrains SAS under R-enriched light (R:FR > 1), while PHYA restrains SAS under FR-enriched light (R:FR < 1) (Franklin, 2008; Lorrain et al., 2008; Franklin and Quail, 2010; Jaillais and Chory, 2010; Martinez-Garcia et al., 2010; Stamm and Kumar, 2010). This also result in the inactivation of PIF to promote BR and auxin production (Martínez et al., 2018a).

The amalgamation of photochemical and non-photochemical processes (NPQ) dissipates excess excitation energy (EEE) of plants as heat. Photochemical- and NPQ-dissipated EEE maintenance is facilitated by the acidification of the chloroplast lumen, involving PSII-associated proteins (Niyogi, 2000; Müller et al., 2001; Li et al., 2004; Niyogi et al., 2005; Ciszak et al., 2015). EEE eventually results in the formation of ROS, H₂O₂, superoxide (O2.-), and singlet oxygen (¹O₂), which overlaps with biotic stress signaling. Light/dark alterations induce plant resistance to pathogen infection and oxidative damage in systemic tissues. This indicates a cross-wired signaling between dark/light conditions and biotic stress (Rossel et al., 2007; Mühlenbock et al., 2008; Szechyńska-Hebda et al., 2010; Zhao et al., 2014). EEE induces SAR and basal response to pathogenic biotrophic bacteria. This response alters ROS and redox signals and thus induces SA, ET, and glutathione (Mühlenbock et al., 2008; Szechyńska-Hebda et al., 2010).

Accumulating evidences indicate that plant response to biotic stress cannot be fully deciphered by studying discrete stress response (Suzuki et al., 2014; Dworak et al., 2016). Such notions support comprehensive study in connection with plant responses to simultaneously appearing stresses. Both qualitative and quantitative changes occur in the intensity of light during dark/light alterations. The majority of invertebrate herbivores with few exceptions (Kreuger and Potter, 2001; VanLaerhoven et al., 2003) are more active at night in comparison with day because of parasitism or predation constraints during the day (Hassell and Southwood, 1978). The emission of volatiles also affects herbivory with respect to diurnal variation. There are even qualitative and quantitative disparities during day/night in wound-induced volatiles (De Moraes et al., 2001; Gouinguené and Turlings, 2002; Martin et al., 2003). Taking into account the effect of dark/light on pathogen attack upon plants, the number of airborne fungal spores is significantly high at night (dark) in comparison with day (Schmale and Bergstrom, 2004; Gilbert and Reynolds, 2005; Zhang et al., 2005). On the contrary, few fungal spores peak at day (light) time (Gadoury et al., 1998; Su et al., 2000). Along with dark/light alterations, the plant–pathogen interaction is also influenced by an array of factors such as temperature fluctuations, humidity changes, and leaf surface water content resulting from dew conditions at night (Meijer and Leuchtmann, 2000; Koh et al., 2003). The presence of light also reduces germ tube growth and spore germination in plant pathogenic fungi (Mueller and Buck, 2003; Beyer et al., 2004). A number of studies have revealed that pathogen infection is influenced by light/dark conditions before inoculation happens. Tolerance to aphid infestation was also confirmed by high-light pre-exposures in wild-type plants and mutants impaired in protein phosphatase 2A (PP2A) (Rasool et al., 2014). Similarly, inoculation of Puccinia striiformis in wheat (Triticum aestivum) seedlings was more at low light intensity than dark-grown seedlings (De Vallavieille-Pope et al., 2002). In a few other instances, inoculation irradiances have been found to be inversely proportional to infection (Shafia et al., 2001), indicating a direct impact of dark/light on host tolerance. Recently, nucleotide-binding NLR Rpi-vnt1.1 proteins have been shown to require light for imparting disease resistance against races of the Irish potato famine pathogen Phytophthora infestans, which discharge the effector protein AVRvnt1 (Gao et al., 2020). Glycerate 3-kinase (GLYK), which is a nuclear-encoded chloroplast protein, is necessary for the activation of Rpi-vnt1.1. Under light conditions, AVRvnt1 binds to the full-length chloroplast targeted GLYK isoform triggering of Rpi-vnt1.1. However, under the dark scenario, plants generate a shorter truncated GLYK that is devoid of the intact chloroplast transit peptide, thus compromising Rpi-vnt1.1-mediated resistance. The conversion between full-length and short-length GLYK transcripts is governed by light-dependent promoter selection mechanism. In plants that are devoid of Rpi-vnt1.1, the occurrence of AVRvnt1 decreases GLYK accumulation in chloroplasts, hence reducing GLYK contribution to basal immunity. The findings are thus clearly depictive of the fact that the pathogen-driven functional alteration of the chloroplast results in a light-dependent immune response (Gao et al., 2020). Plausibly, plants are more prone to pathogen attack in the dark than during the day. However, it cannot be held true for all pathogens attacking the plant systems.

There occur two mechanisms that contribute to the regulation of plant defense responses during dark/light fluctuations: first, the energetic significance of light-dependent chemical reactions (depends on the capacity of photosynthetic electron transport to produce ATP and reducing power); and second, perception of light (shade and R:FR exposure conditions) and regulation of downstream light-dependent signaling pathways (Roberts and Paul, 2006). The following subsections highlight both the mechanisms with respect to photosynthesis, ROS accumulation, and light signaling.

Exposure of plants to a combination of adverse environmental cues such as biotic stresses and light fluctuations coerces the efforts to meet enormous food demand. Despite the massive usage of pesticides and insecticides in the last few decades, the overall crop losses due to pathogen attack have not been reduced significantly. Monitoring infection time, plant growth, and other important parameters such as light/dark conditions can result in a better understanding of plant defense toward pathogens, particularly when extrapolated to field conditions. The present review provides an elaborate information on how plants perceive and respond to multiple dark/light alterations and biotic stresses. Light and dark conditions together or independently modulate a diverse range of signaling pathways to control pivotal plant growth and defense regulators. The function of multi-faceted dark/light signaling intermediates such as COP, CRY, PHY, and PIF has been extensively covered to highlight the impact of dark and light modulations on plant biotic defense responses. Even though significant efforts have been made to deep dive into the plant–microbe interactions and their association with light signaling, the mechanistic details encircling this complex intersection are obscure. Thus, the basic research to comprehend the mechanisms involved in the integrated circuitry of plant immunity and dark/light interactions, at both biological and ecological scales, will pave the way to overcome the limitations associated with crop losses globally.

MIA conceptualized and designed the study. ZI, MSI, AH, and EFA compiled the data and wrote the manuscript. All authors have read the manuscript and agreed for publication.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.