Signaling mechanisms and biochemical pathways regulating pollen-stigma interaction, seed development and seedling growth in sunflower under salt stress

Figures & data

Table 1. Molecular markers of stigma maturation in sunflower^12–14.

Stages of stigma development	Associated markers/events	Possible roles
Bud stage to Staminate stage	Production of extracellular lipid-rich secretions	Maintains semi-dry nature of stigma
	Potassium accumulation	Maintaining turgidity in stigma
	Carbohydrate accumulation	Nutrients for pollination
Staminate stage to Pistillate stage	Beginning of pollen adhesion on stigma surface
	β-1,3 glucanase activity increases	Helps in distribution of callose
	Expression of lipase activity	Causes accumulation of unsaturated fatty acids to maintain semi-dry nature of mature stigma
	Enhanced expression of fatty acyl esterase activity	Facilitates cutinase complex formation with pollen surface, thus aiding pollen tube penetration
	ROS and NO accumulation	Provide enhanced immunity to maturing stigma

Figure 1. NO-modulated ethylene and SL biosynthesis and possible causes of their impact on lateral root formation

Abbreviations: ACC oxidase – Aminocyclopropanecarboxylate oxidase; CCD – Carotenoid cleavagedioxygenase.²³

Figure 2. Proposed model of fatty acid biosynthesis in sunflower achenes and modulation of its composition as a response to 120 mM NaCl

Salt stress begins with the uptake of Na⁺ from the soil which affects the profuseness of lateral roots. In salt-sensitive variety, Na⁺ rapidly move and accumulate in the aerial plant parts via long distance signaling. Accumulation of Na⁺ in the achenes leads to noteworthy changes in K⁺ and Ca⁺² accumulation in the cell. These changes in the ionic status disturb the fatty acid biosynthesis. Saturated fatty acids, palmitic (16:0) and stearic acid (18:0) are either further elongated by elongases (Eln) to form very long chain fatty acids (VLCFAs), such as eicosanoic acid (20:0) or docosanoic acid (22:0) or double bonds are added by desaturases (ΔD) to position 9 or 11 to form oleic acid (18:1Δ⁹) and cis-vaccenic acid (18:1Δ¹¹), respectively. Oleic acid is further converted to linoleic acid (18:1Δ^9,12), which is further converted to linolenic acid (18:1Δ^9,12,16) by the action of membrane bound desaturases. These fatty acids are further involved in several physiological pathways like TAG de novo synthesis in ER, regulation of phospholipase-D, NO-mediated defense pathway, hexanoic acid (Hx)- mediated regulation of JA and SA- mediated defense pathways.

Figure 3. An overview of differential expression pattern of NO, ROS, post-translational protein modifications (tyrosine nitration and S-nitrosylation) and organeller abundance in 2 d old salt-tolerant and sensitive seedlings in response to salt stress, NO donor and NO scavenger

DETA is the NO donor whereas DETC is the scavenger of NO. Length of arrows indicates their relative expression or accumulation patterns as compared to control. Abbreviations: Mit.- mitochondria; Nuc.- nucleus; OBMP- oil body membrane protein; Per.-peroxisome; ROS- reactive oxygen species; S-NO- S-Nitrosylation; Tyr. NO2- tyrosine nitration.

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