Given a context passage, generate a question from the passage such that its answer is shortest continous span from the passage.

Your respiratory system is made up of the tissues and organs that allow oxygen to enter your body and carbon dioxide to leave your body. Organs in your respiratory system include your: Nose. Mouth. Larynx. Pharynx. Lungs. Diaphragm. The organs of the respiratory system move air into and out of the body. These structures are shown below (Figure 1.1). What do you think is the purpose of each of these organs? The nose and the nasal cavity filter, warm, and moisten the air you breathe. The nose hairs and the mucus produced by the cells in the nose catch particles in the air and keep them from entering the lungs. Behind the nasal cavity, air passes through the pharynx, a long tube. Both food and air pass through the pharynx. The larynx, also called the "voice box," is found just below the pharynx. Your voice comes from your larynx. Air from the lungs passes across thin tissues in the larynx and produces sound. The trachea, or windpipe, is a long tube that leads down to the lungs, where it divides into the right and left bronchi. The bronchi branch out into smaller bronchioles in each lung. There is small flap called the epiglottis that covers your trachea when you eat or drink. The muscle controlling the epiglottis is involuntary and prevents food from entering your lungs or wind pipe. The bronchioles lead to the alveoli. Alveoli are the little sacs at the end of the bronchioles (Figure 1.2). They look like little bunches of grapes. Oxygen is exchanged for carbon dioxide in the alveoli. That means oxygen enters the blood, and carbon dioxide moves out of the blood. The gases are exchanged between the blood and alveoli by simple diffusion. The diaphragm is a sheet of muscle that spreads across the bottom of the rib cage. When the diaphragm contracts, the chest volume gets larger, and the lungs take in air. When the diaphragm relaxes, the chest volume gets smaller, and air is pushed out of the lungs. "Grape-like" alveoli in the lungs.
what keeps food out of the lungs?

In eukaryotic cells, there are two sub-pathways of nucleotide excision repair (NER), the global genome (gg) NER and the transcription-coupled repair (TCR). TCR can preferentially remove the bulky DNA lesions located at the transcribed strand of a transcriptional active gene more rapidly than those at the untranscribed strand or overall genomic DNA. This strand-specific repair in a suitable restriction fragment is usually determined by alkaline gel electrophoresis followed by Southern blotting transfer and hybridization with an indirect end-labeled single-stranded probe. Here we describe a new method of TCR assay based on strand-specific-PCR (SS-PCR). Using this method, we have investigated the role of DNA-dependent protein kinase catalytic subunit (DNA-PKcs), a member of the phosphatidylinositol 3-kinase-related protein kinases (PIKK) family, in the TCR pathway of UV-induced DNA damage. Although depletion of DNA-PKcs sensitized HeLa cells to UV radiation, it did not affect the ggNER efficiency of UV-induced cyclobutane pyrimidine dimers (CPD) damage. We postulated that DNA-PKcs may involve in the TCR process. To test this hypothesis, we have firstly developed a novel method of TCR assay based on the strand-specific PCR technology with a set of smart primers, which allows the strand-specific amplification of a restricted gene fragment of UV radiation-damaged genomic DNA in mammalian cells. Using this new method, we confirmed that siRNA-mediated downregulation of Cockayne syndrome B resulted in a deficiency of TCR of the UV-damaged dihydrofolate reductase (DHFR) gene. In addition, DMSO-induced silencing of the c-myc gene led to a decreased TCR efficiency of UV radiation-damaged c-myc gene in HL60 cells. On the basis of the above methodology verification, we found that the depletion of DNA-PKcs mediated by siRNA significantly decreased the TCR capacity of repairing the UV-induced CPDs damage in DHFR gene in HeLa cells, indicating that DNA-PKcs may also be involved in the TCR pathway of DNA damage repair. By means of immunoprecipitation and MALDI-TOF-Mass spectrometric analysis, we have revealed the interaction of DNA-PKcs and cyclin T2, which is a subunit of the human transcription elongation factor (P-TEFb). While the P-TEFb complex can phosphorylate the serine 2 of the carboxyl-terminal domain (CTD) of RNA polymerase II and promote transcription elongation. A new method of TCR assay was developed based the strand-specific-PCR (SS-PCR). Our data suggest that DNA-PKcs plays a role in the TCR pathway of UV-damaged DNA. One possible mechanistic hypothesis is that DNA-PKcs may function through associating with CyclinT2/CDK9 (P-TEFb) to modulate the activity of RNA Pol II, which has already been identified as a key molecule recognizing and initializing TCR.
Which gene strand is targeted by transcription-coupled repair (TCR)?

Rhopalizus is a genus of round-necked longhorn beetles of the subfamily Cerambycinae.

Is Rhopalizus a genus or species?

