Unclasping potentials of genomics and gene editing in chickpea to fight climate change and global hunger threat

Abstract

Genomics and genome editing promise enormous opportunities for crop improvement and elementary research. Precise modification in the specific targeted location of a genome has profited over the unplanned insertional events which are generally accomplished employing unadventurous means of genetic modifications. The advent of new genome editing procedures viz; zinc finger nucleases (ZFNs), homing endonucleases, transcription activator like effector nucleases (TALENs), Base Editors (BEs), and Primer Editors (PEs) enable molecular scientists to modulate gene expressions or create novel genes with high precision and efficiency. However, all these techniques are exorbitant and tedious since their prerequisites are difficult processes that necessitate protein engineering. Contrary to first generation genome modifying methods, CRISPR/Cas9 is simple to construct, and clones can hypothetically target several locations in the genome with different guide RNAs. Following the model of the application in crop with the help of the CRISPR/Cas9 module, various customized Cas9 cassettes have been cast off to advance mark discrimination and diminish random cuts. The present study discusses the progression in genome editing apparatuses, and their applications in chickpea crop development, scientific limitations, and future perspectives for biofortifying cytokinin dehydrogenase, nitrate reductase, superoxide dismutase to induce drought resistance, heat tolerance and higher yield in chickpea to encounter global climate change, hunger and nutritional threats.

Keywords: CRISPR/Cas-9; TALENs; chickpea improvement; climate change; genome editing; hunger threat; zinc finger nuclease.

FIGURE 1

(A) SSRs facilitating DNA strand breakage at two points (pointed boxes) followed by rearranging (“swap”) the broken ends and reconnecting them in the new configuration. (B) A crossover site (light orange box) with inverted repeat symmetry (two blue arrows) binding an SSR dimer and containing the broken bonds and re-joined by the SSR at its centre (typically 30–40 bp). The crossover site could have accessory sites (Green boxes) that bind more SSR and/or regulatory protein subunits.

FIGURE 2

Mechanism of Tyrosine recombinase (A–D), making an intermediate Holliday junction by expurgating and interchanging one pair of DNA strands, followed by cutting and interchanging the other couple of strands.

FIGURE 3

Mechanism of Serine recombinase (A–E) making double-strand breaks in all crossover sites before reshuffling the fragmented DNA ends and rejoining the strands.

FIGURE 4

Diagram depicts the components required for the action of ZFN. It consists of 4–6 zinc finger domain (green and red colour) which binds to the targeted DNA sequence. For the action of FoI enzyme, type II restriction enzyme (yellow colour). Two monomeric sequence attaches on DNA sequence and allow FokI to create double stranded breaks. These breaks will be repaired via non-homology end joining or Homology directed repair method.

FIGURE 5

TALE activator along with a pair of TALENs.

FIGURE 6

Generalized mechanism of CRISPR/Cas-9.

FIGURE 7

Limitations and benefits of CRISPR technology.

FIGURE 8

Generalized mechanism of base editing.

FIGURE 9

Mechanism of prime editing.