Global Journal of Science Frontier Research, G: Bio-Tech & Genetics, Volume 22 Issue 2

however, it is only optimum physiological relevant concentration of sucrose that maintain strong inhibition of SnK1 activity (168, 169). Furthermore, SnRK1 negatively interact with another sugar growth promoting signaling pathway regulator (target of rapamycin) TOR in regulation of plant sugar and growth. SnRK1 downregulates the activities of TOR by phosphorylation of key enzymes involved in nitrogen and carbon metabolism through bZIP transcription factors, thereby decrease TOR activity that causes accumulation of sugars and amino acids (170-172). Thereby revealing the integration of activities of sugar sufficient growth promoting signaling pathway ( T6P; TOR ) and sugar deficient growth inhibition signaling pathway ( SnRK1 ) plant growth and development regulation. Figure 6 below shows the two glucose pathways and their crosstalk with plant phytohormones in dormancy regulation SnRK1 is also a key player in crosstalk between sugar signaling pathways and hormonal regulatory networks in dormancy induction and regulation. For example, in Pea, postembryonic silencing of SnRk1 α through a seed storage protein promoter result in defective cotyledon development and seed maturation, including reduced accumulation of protein reserves, impaired desiccation tolerance and viviparity (173, 174). These effects have been reported to be accompanied by altered expression of genes related to cell proliferation and differentiation, leaf polarity and seed maturation, such as FUSCA3 and ABI3 (170). Also, SnRK1 repression reduces the accumulation of cytokinin and ABA (173), thereby impacting on the auxin/cytokinin ratio, another critical factor in plants’ decision on root and shoot growth and revealing a link between sugar signaling pathways and hormonal regulatory networks in dormancy induction. In in vitro study, SnRK1 phosphorylates FUSCA3 transcription factor, but FUSCA3 degradation was delayed in cell extracted from 35S:SnRK1 α 1 mutant plants. Furthermore, 35S:SnRK1 α 1 fusca3-3 double mutant plants display precocious germination and desiccation intolerance similar to fusca3-3 single mutant plants (158, 170), indicating that SnRK1 induce dormancy by stabilizing FUSCA3 . Sugar signaling-ABA induced growth arrest phenotype in Arabidopsis has been screened on high sugar containing medium (6% glucose). This has led to elegant characterization of mutants that are insensitive to sugars. Surprisingly, many of these mutants have defects in ABA biosynthesis or signaling (175), in fact the allelic mutants were identified to be ABA synthesis (aba) and ABA insensitive (abi) in Arabidopsis (176). The role of ABA in plant glucose signaling was described by the characterization of glucose insensitive 5 (gin5) and glucose insensitive 6 ( gin6 )/sucrose uncoupling 6 ( sun6 )/ sugar insensitive 5 ( sin5 ) as mutant alleles of aba3 and abi4 respectively (177, 178). In addition, while ABA insensitive 5 ( abi5 ) displayed a glucose insensitive phenotype, over expression of ABI5 results in hypersensitivity to sugars(179, 180). Also, ABI5 encodes a transcript factor that belongs to the basic leucine zipper (b/ZIP ) family, and ABA-responsive element binding factors ABF3 and ABF4, two members of b/ZIP domain family are strongly induced by ABA (179, 181), suggesting that the role of ABI5 in glucose-mediated dormancy induction partially overlaps with those other b/ZIP factors(175) (182). Two models can possibly explain the overlap between sugar and ABA signaling. That high sugar levels may trigger enhanced ABA synthesis which in turn activates ABA signaling, or that ABA signaling activates shared targets of a separate sugar signaling pathway. This synergistic interaction between ABA and sugar signaling is supported by the fact that ABA alone cannot regulate the expression of some sugar-dependent genes, although it has defining enhancing effect when provided with sucrose (183). © 2022 Global Journals 1 Year 2022 64 Global Journal of Science Frontier Research Volume XXII Issue ersion I VII ( G ) Physiological and Molecular basis of Dormancy in Yam Tuber: A Way Forward towards Genetic Manipulation of Dormancy in Yam Tubers