The plant hormone ethylene regulates variety of growth and developmental processes including germination, seedling growth, organ senescence, organ abscission, and fruit ripening. The established pathway for ethylene signaling involves ethylene perception by a family of five ethylene receptors ETR1, ERS1, ETR2, ERS2 and EIN4 (Hua et al. 1998) related to the bacterial histidine kinases and residing in Endoplasmic Reticulum (ER) membrane (Chen et al. 2002, Grefen et al. 2008). Ethylene receptors associate and regulate the Raf-like protein kinase CTR1 (Clark et al. 1998, Gao et al. 2003), which is positioned downstream of the ethylene receptors in signaling pathway based on epistasis analysis and act as a negative regulator of ethylene signaling. Further downstream regulators include EIN2, a small family of EIN3, EIN3-like proteins and ERF1 which belongs to a large ERF super-family (Nakano et al. 2006). There are numerous mechanisms which can modulate the output of ethylene signaling pathway and in turns regulate the sensitivity of plants towards ethylene (Binder et al. 2012), like transcriptional regulation and, clustering of receptors (Gao et al. 2008, Grefen et al. 2008, Gao et al. 2009), and interactions of pathway elements with auxiliary proteins such as the RTE1/GR family (Barry et al. 2006, Resnick et al. 2006). In addition, various genes have also been identified as modulating the ethylene response based on a genetic screen for enhanced ethylene sensitivity (Larsen et al. 2001, Larsen et al. 2003, Christians et al. 2007, Robles et al. 2007, Christians et al. 2008). Our work explores two important regulatory mechanisms involved in ethylene signaling in Arabidopsis; (i) the regulation of CTR1 in response to ethylene and (ii) the characterization of the novel role of ARGOS gene family as negative feedback mediators of ethylene signaling. Genetic studies propose that hormone binding leads to inactivation and most likely the degradation of ethylene receptors, which are negative regulators of signaling pathway (Hua et al. 1998, Tieman et al. 2000). When active, that is in the absence of ethylene, the receptors suppress ethylene responses. Presence of ethylene inactivates the receptors, to trigger ethylene signaling resulting in ethylene responses. Ligand induced proteasome mediated degradation of ethylene receptors has also been reported (Chen et al. 2007). Ethylene receptors as well as Raf-like kinase CTR1 are acting as negative regulators of ethylene signaling. CTR1 is itself a soluble protein Regulators of Ethylene Signaling in Arabidopsis thaliana: CTR1 and ARGOS Family having no transmembrane domains but is found in membranes, because it is bound to receptors which are present in ER membrane. Receptor degradation in response to ethylene binding generates questions about the fate of CTR1 afterwards. Our data support a model in which perception of ethylene results in the production of new CTR1 largely through transcriptional induction, but ethylene also induces post transcriptional modifications in CTR1 in such a way that levels of CTR1 at the membrane drops in response to ethylene. Apart from CTR1 role in the established ethylene signaling network, we report novel role of ARGOS (AUXIN REGULATED GENE INVOLVED IN ORGAN SIZE) gene family being a negative regulators of ethylene signaling. ARGOS gene family consists of four protein members ARGOS, ARL, OSR1 and OSR2. ARGOS, as its name indicates, is previously reported to be induced in response to auxin (Hu et al. 2003), here we report their main role is to serve as negative feedback mediators of ethylene signaling. We provide evidences of the prominent induction of all four members of ARGOS family in response to ethylene where induction levels varies, suggesting a range of their role in response to various levels of ethylene concentration. Ethylene insensitive mutants abolish the response of ARGOS family which further supports their role in ethylene signaling. The transcript induction of ARGOS and ARL is parallel to the levels of induction of ethylene receptors. Genetic analysis provide evidence that over expression of ARGOS and ARL enhances negative regulation in ethylene signaling, reducing ethylene sensitivity based on both physiological and molecular responses, supporting their place in ethylene negative feedback loop.
The study critically engages with the issue of continuity of the orientalist rhetoric in the contemporary literary yields. To establish and substantiate the argument, the researchers have analyzed Deborah Ellis’s Breadwinner Trilogy (2009) that comprises Breadwinner, Parvana’s Journey, and Mud City. All the three fictional narratives claims to have represented the life of the Pakistani and Afghani characters who have been shown to face the existential threats in the wake of the insecurities that have engulfed the region. However, the study contends, the Canadian writer has also given way to the parochial psychological and sociological schema that has been held as the prime representational trope regarding the East, that is, Orientalism. The qualitative and textual approach has facilitated the researchers to negotiate the identified thematic patterns with the interpretive freedom. In this regard, framing the fictional representation into the Saidian critique of the orientalist discourse, the study explicates the reductive approach of the writer and exposes the latent ideological triggers working under the manifest humanist projections. Thus, the study strengthens the postcolonial stance and, therefore, will sharpen the Pakistani students’ understanding of the current socio-literary debates.
In this thesis, a novel technique to embed synaptic plasticity in neuromorphic hardware is proposed named as Frequency Dependent Synaptic Plasticity. This technique provides an alternate interpretation for plasticity which was conventionally modeled as weight value. In the proposed model of neuromorphic hardware, plasticity is implemented in frequency domain by considering a synaptic connection performing bandpass filtering operation. Currently most of the neuromorphic hardware are based on time domain based plasticity techniques. The proposed model attempts to contribute and suggest an out of the box solution for neurocomputational applications. It has been established through this thesis that the proposed model is biologically plausible in terms of implementation of different phenomena observed in a biological brain such as rate-encoding by Class I type of neuron, decoding of rate-encoded information by selective triggering at post synaptic side, resonance aware synaptic plasticity, population coding, role and interpretation of tuning curve, and frequency based neuronal communication. The proposed hardware operates in analog domain which is closer to the operational domain of brain as compared to its digital counterpart. This thesis also proposes a novel architecture to embed population coding on neuromorphic hardware. Further, it is explained in this thesis that a synaptic junction based on proposed model has a non linear transfer function which omits the requirement of hidden layer in classifying non-linear problems. This will allow applications to use least possible resources, employing input and output nodes only, as compared to a network based on linear weight values.