The soybean cyst nematode (SCN), Heterodera glycines, a plant parasitic pest, causes severe yield losses of soybean (Glycine max). Although a number of studies have identified various genes that function in defense, including a role for the vesicular transport machinery acting against H. glycines in infected roots, a regulatory mechanism occurring behind the transcriptional engagement of the vesicular transport system and delivery of the transported cargo proteins is not fully understood. The main goal of the current study is to determine the functional effect of genetically engineering the circadian clock gene, CIRCADIAN CLOCK ASSOCIATED 1 (CCA1) in G. max to examine a role on H. glycines parasitism. The outcome of the study has determined the functional effect of main clock component CCA1-1 along with other oscillator genes such as TIMING OF CAB 1 (TOC1-1), GIGANTEA (GI-1) and CONSTANS (CO-4) to enhance resistance against H. glycines parasitism. Further, the reduced level of the expression of Gm-CCA1-1 in infected roots, in comparison to uninfected roots, has demonstrated that clock components might have arrested and altered its expression during the nematode infection process. The study has also investigated the role of XYLOGLUCAN ENDO-TRANSGLYCOSYLASE /HYDROLASE (XTH), Gm-XTH43, during the resistance process soybean has to H. glycines. The results have demonstrated higher xyloglucan (XyG) amounts to be synthesized in the Gm-XTH43 overexpressing (OE) lines. In contrast, there is less XyG in the Gm-XTH43 RNA interference (RNAi) lines that have a negatively regulated XTH gene. These observations have led to elucidating the role in the potential cell wall rearrangement and the underlying metabolic processes required for the generation of the proper XyG architecture required for defense occurring outside of the plant cell. Furthermore, the observed result of lower level of weight average molecular weight (WAMW) of XyG in Gm-XTH43-OE and higher MW of XyG in Gm-XTH43-RNAi than respective control roots have demonstrated a key role in, presumably, changing the cell wall by the remodeling of the XyG chain as it relates to the cell wall architecture.